human escc cell line kyse30 Search Results


93
ATCC human escc cell lines kyse30
Human Escc Cell Lines Kyse30, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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JCRB Cell Bank kyse-30
A 3 × 10 6 KYSE-30 cells were subcutaneously inoculated into BALB/c nude mice to establish the S.C. tumor model, and then 1 × 10 7 PFU of rMV-Hu191 were administrated intratumorally (I.T.) from day 12 to day 17. B Tumors were measured in the long and short dimensions using a vernier caliper, and tumor volumes were estimated using the equation: V = (length × Width 2 )/2. n = 8 tumors for each group. * p < 0.05, **** p < 0.0001, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. C Difference in tumor volume on day 27 post tumor cell inoculation. * p < 0.05, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. D The Kaplan–Meier survival curves of mice from rMV-Hu191 and mock-treated groups. A log-rank (Mantel–Cox) test was used to analyze the significance of differences between groups. *** p < 0.0001. E Body weights of the mock and rMV-Hu191-treated mice were measured on day 0 and 15 post virus injection. The solid line represents the average weight ± SEM ( n = 8). ns, no significant differences, two-tailed Student’s t -test. F – H The levels of ALT, AST and CR in mouse serum were measured. Data are presented as mean ± SEM ( n = 3). ns, no significant differences, two-tailed Student’s t -test. I , J Immunofluorescence staining of the mock and rMV-Hu191-treated tumors with the indicated antibodies. The scale bars represent 50 μm. K Immunoblot analysis revealed elevated GSDME cleavage in rMV-Hu191-treated tumors. L Schematic model for the regulation of pyroptosis in <t>ESCC</t> by rMV-Hu191. rMV-Hu191 exhibits an antitumor effect through BAK/BAX-dependent caspase-3/GSDME-mediated pyroptosis.
Kyse 30, supplied by JCRB Cell Bank, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
DSMZ human escc cell lines
A 3 × 10 6 KYSE-30 cells were subcutaneously inoculated into BALB/c nude mice to establish the S.C. tumor model, and then 1 × 10 7 PFU of rMV-Hu191 were administrated intratumorally (I.T.) from day 12 to day 17. B Tumors were measured in the long and short dimensions using a vernier caliper, and tumor volumes were estimated using the equation: V = (length × Width 2 )/2. n = 8 tumors for each group. * p < 0.05, **** p < 0.0001, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. C Difference in tumor volume on day 27 post tumor cell inoculation. * p < 0.05, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. D The Kaplan–Meier survival curves of mice from rMV-Hu191 and mock-treated groups. A log-rank (Mantel–Cox) test was used to analyze the significance of differences between groups. *** p < 0.0001. E Body weights of the mock and rMV-Hu191-treated mice were measured on day 0 and 15 post virus injection. The solid line represents the average weight ± SEM ( n = 8). ns, no significant differences, two-tailed Student’s t -test. F – H The levels of ALT, AST and CR in mouse serum were measured. Data are presented as mean ± SEM ( n = 3). ns, no significant differences, two-tailed Student’s t -test. I , J Immunofluorescence staining of the mock and rMV-Hu191-treated tumors with the indicated antibodies. The scale bars represent 50 μm. K Immunoblot analysis revealed elevated GSDME cleavage in rMV-Hu191-treated tumors. L Schematic model for the regulation of pyroptosis in <t>ESCC</t> by rMV-Hu191. rMV-Hu191 exhibits an antitumor effect through BAK/BAX-dependent caspase-3/GSDME-mediated pyroptosis.
Human Escc Cell Lines, supplied by DSMZ, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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YUTAKA Engineering Corporation human escc cell lines kyse510
Clinical information of <t> ESCC </t> patients.
Human Escc Cell Lines Kyse510, supplied by YUTAKA Engineering Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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HybriBio Limited cell line kyse30
Up-regulated LINC00673 is associated with poor prognosis in esophageal squamous cell carcinoma <t>(ESCC)</t> patients. (A) LINC00673 expression levels were evaluated using quantitative PCR (qPCR) in 39 pairs of ESCC tissues and corresponding non-tumor tissues. *** P < 0.001 (unpaired Student’s t test). (B) Receiver operating characteristic (ROC) curve of LINC00673 in 39 ESCC patients. (C–E) Relationships between LINC00673 expression and the differentiation grade, tumor size, and lymph node metastasis, respectively. (F) Kaplan–Meier curves show the survival of ESCC patients, as grouped by the LINC00673 expression levels. * P < 0.05.
Cell Line Kyse30, supplied by HybriBio Limited, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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iCell Bioscience Inc human escc cell lines (kyse30, kyse410, kyse150, and te-1 cells)
Up-regulated LINC00673 is associated with poor prognosis in esophageal squamous cell carcinoma <t>(ESCC)</t> patients. (A) LINC00673 expression levels were evaluated using quantitative PCR (qPCR) in 39 pairs of ESCC tissues and corresponding non-tumor tissues. *** P < 0.001 (unpaired Student’s t test). (B) Receiver operating characteristic (ROC) curve of LINC00673 in 39 ESCC patients. (C–E) Relationships between LINC00673 expression and the differentiation grade, tumor size, and lymph node metastasis, respectively. (F) Kaplan–Meier curves show the survival of ESCC patients, as grouped by the LINC00673 expression levels. * P < 0.05.
Human Escc Cell Lines (Kyse30, Kyse410, Kyse150, And Te 1 Cells), supplied by iCell Bioscience Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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China Center for Type Culture Collection human escc cell line kyse450
Dihydrotanshinone I inhibits proliferation of esophageal squamous cell carcinoma cells while showing no proliferation inhibition in normal esophageal epithelial cells. A-E: Cell viability of esophageal squamous cell carcinoma cells <t>(KYSE30,</t> Eca109, KYSE-450, and KYSE-510) and normal esophageal epithelial cells (Het-1A) after treatment with dihydrotanshinone I for 12 h, 24 h, and 36 h. DHTS: Dihydrotanshinone I.
Human Escc Cell Line Kyse450, supplied by China Center for Type Culture Collection, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Procell Inc human escc cell line kyse30
PRDX4 exhibits high expression in <t>ESCC</t> tissues and cells. (A) Sangerbox 3.0 online software assay for PRDX4 expression in pan-cancer. (B) UALCAN database investigation for PRDX4 expression in ESCA samples and normal esophageal epithelial tissues. (C) GEO dataset GSE111011 was used to investigate the expression of PRDX4 in ESCC samples and paired normal samples. (D) RT-qPCR assay was used to assess the expression of PRDX4 in 65 ESCC samples and paired normal samples. (E) Western blot analysis of the protein expression of PRDX4 in eight ESCC samples and paired normal samples. (F) The relative protein levels of PRDX4 in eight ESCC samples and paired normal samples. (G) IHC detection of PRDX4 expression in normal tissues and ESCC tissues. Scale bar, 20 µm. (H) Western blot analysis of PRDX4 protein expression in ESCC cell lines (KYSE70, KYSE450, KYSE520, <t>KYSE30</t> and KYSE270) and normal esophageal epithelial cell line Het-1A. (I) The relative protein levels of PRDX4 in ESCC cell lines and Het-1A cells. (J) RT-qPCR assay of PRDX4 mRNA expression in the aforementioned ESCC cell lines and Het-1A cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; ns, not significant.
Human Escc Cell Line Kyse30, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
YUTAKA Engineering Corporation human escc cell lines kyse30
PRDX4 exhibits high expression in <t>ESCC</t> tissues and cells. (A) Sangerbox 3.0 online software assay for PRDX4 expression in pan-cancer. (B) UALCAN database investigation for PRDX4 expression in ESCA samples and normal esophageal epithelial tissues. (C) GEO dataset GSE111011 was used to investigate the expression of PRDX4 in ESCC samples and paired normal samples. (D) RT-qPCR assay was used to assess the expression of PRDX4 in 65 ESCC samples and paired normal samples. (E) Western blot analysis of the protein expression of PRDX4 in eight ESCC samples and paired normal samples. (F) The relative protein levels of PRDX4 in eight ESCC samples and paired normal samples. (G) IHC detection of PRDX4 expression in normal tissues and ESCC tissues. Scale bar, 20 µm. (H) Western blot analysis of PRDX4 protein expression in ESCC cell lines (KYSE70, KYSE450, KYSE520, <t>KYSE30</t> and KYSE270) and normal esophageal epithelial cell line Het-1A. (I) The relative protein levels of PRDX4 in ESCC cell lines and Het-1A cells. (J) RT-qPCR assay of PRDX4 mRNA expression in the aforementioned ESCC cell lines and Het-1A cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; ns, not significant.
Human Escc Cell Lines Kyse30, supplied by YUTAKA Engineering Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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YUTAKA Engineering Corporation yes-2
The expression of BAALC‐AS1 in <t>ESCC.</t> A. In situ hybridization of BALC‐AS1 in <t>ESCC</t> tissue samples and their corresponding adjacent normal tissues. Scale bar: left, 100 μm; right, 200 μm. Adjacent, adjacent normal tissues; Cancer, ESCC tissues. B. Comparison of BAALC‐AS1 scores of ESCC and adjacent normal tissues. C. ESCC patients with high levels of BAALC‐AS1 expression showed reduced survival compared with those with low levels of BAALC‐AS1 expression ( P = 0.037; log‐rank test). D. Differences in the overall survival and pathological stage between patients with high BAALC‐AS1 expression level and low BAALC‐AS1 expression level were highly significant. E. Expression of BAALC‐AS1 quantified by RT‐qPCR in ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510, and COLO‐680) and normal esophageal epithelial cell line (Het‐1A). F. Analysis of BAALC‐AS1 distribution by cellular fractionation followed RT‐qPCR in KYSE‐510 cells. U6 and 18s mRNAs were served as controls for nuclear and cytoplasmic RNAs, respectively. G. RNA‐ FISH was performed to detect BAALC‐AS1 expression in KYSE‐510 cells. The nuclei were counterstained with 4′,6‐diamidino‐2‐phenylindole (DAPI). Scale bar, 10 μm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. All of the values are expressed as the mean ± SEM of 3 experiments
Yes 2, supplied by YUTAKA Engineering Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Servicebio Inc kyse30 human escc cell line
Spatial whole-transcriptome profiling of ESPL and <t>ESCC</t> samples (A) Workflow of DSP experimental process. (B) The UMAP plot displaying the clustering results of AOIs from different compartments at multiple stages of ESCC. (C) The heatmap displaying the expression levels of AOI characteristic markers RNA in different compartments. (D) The boxplots showing the expression levels of marker genes in five different compartments at different stages of ESCC. Box plot shows the median and interquartile range, whiskers extend to 1.5 × IQR. DSP, digital spatial profiling; UMAP, uniform manifold approximation and projection; AOI, area of interest; EP, epithelial-cell-enriched; MC, macrophage-cell-enriched; NC, neutrophil-cell-enriched; ST, stroma-enriched; LS, lymphoid structure; CAFs, cancer-associated fibroblasts; ESPL, esophageal squamous precancerous lesion; non-mESCC, non-metastasis esophageal squamous cell carcinoma; mESCC, metastasis esophageal squamous cell carcinoma; mLN, lymph node metastasis tissues.
Kyse30 Human Escc Cell Line, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A 3 × 10 6 KYSE-30 cells were subcutaneously inoculated into BALB/c nude mice to establish the S.C. tumor model, and then 1 × 10 7 PFU of rMV-Hu191 were administrated intratumorally (I.T.) from day 12 to day 17. B Tumors were measured in the long and short dimensions using a vernier caliper, and tumor volumes were estimated using the equation: V = (length × Width 2 )/2. n = 8 tumors for each group. * p < 0.05, **** p < 0.0001, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. C Difference in tumor volume on day 27 post tumor cell inoculation. * p < 0.05, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. D The Kaplan–Meier survival curves of mice from rMV-Hu191 and mock-treated groups. A log-rank (Mantel–Cox) test was used to analyze the significance of differences between groups. *** p < 0.0001. E Body weights of the mock and rMV-Hu191-treated mice were measured on day 0 and 15 post virus injection. The solid line represents the average weight ± SEM ( n = 8). ns, no significant differences, two-tailed Student’s t -test. F – H The levels of ALT, AST and CR in mouse serum were measured. Data are presented as mean ± SEM ( n = 3). ns, no significant differences, two-tailed Student’s t -test. I , J Immunofluorescence staining of the mock and rMV-Hu191-treated tumors with the indicated antibodies. The scale bars represent 50 μm. K Immunoblot analysis revealed elevated GSDME cleavage in rMV-Hu191-treated tumors. L Schematic model for the regulation of pyroptosis in ESCC by rMV-Hu191. rMV-Hu191 exhibits an antitumor effect through BAK/BAX-dependent caspase-3/GSDME-mediated pyroptosis.

Journal: Cell Death Discovery

Article Title: Recombinant measles virus vaccine rMV-Hu191 exerts an oncolytic effect on esophageal squamous cell carcinoma via caspase-3/GSDME-mediated pyroptosis

doi: 10.1038/s41420-023-01466-2

Figure Lengend Snippet: A 3 × 10 6 KYSE-30 cells were subcutaneously inoculated into BALB/c nude mice to establish the S.C. tumor model, and then 1 × 10 7 PFU of rMV-Hu191 were administrated intratumorally (I.T.) from day 12 to day 17. B Tumors were measured in the long and short dimensions using a vernier caliper, and tumor volumes were estimated using the equation: V = (length × Width 2 )/2. n = 8 tumors for each group. * p < 0.05, **** p < 0.0001, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. C Difference in tumor volume on day 27 post tumor cell inoculation. * p < 0.05, two-tailed Student’s t -test. The solid line represents the average volume ± SEM. D The Kaplan–Meier survival curves of mice from rMV-Hu191 and mock-treated groups. A log-rank (Mantel–Cox) test was used to analyze the significance of differences between groups. *** p < 0.0001. E Body weights of the mock and rMV-Hu191-treated mice were measured on day 0 and 15 post virus injection. The solid line represents the average weight ± SEM ( n = 8). ns, no significant differences, two-tailed Student’s t -test. F – H The levels of ALT, AST and CR in mouse serum were measured. Data are presented as mean ± SEM ( n = 3). ns, no significant differences, two-tailed Student’s t -test. I , J Immunofluorescence staining of the mock and rMV-Hu191-treated tumors with the indicated antibodies. The scale bars represent 50 μm. K Immunoblot analysis revealed elevated GSDME cleavage in rMV-Hu191-treated tumors. L Schematic model for the regulation of pyroptosis in ESCC by rMV-Hu191. rMV-Hu191 exhibits an antitumor effect through BAK/BAX-dependent caspase-3/GSDME-mediated pyroptosis.

Article Snippet: The human ESCC cell lines KYSE-30, KYSE-150 and KYSE-510 were from the JCRB cell bank (Japanese Collection of Research Bioresources cell bank) and cultured in RMPI 1640 (GIBCO) supplemented with 10% fetal bovine serum (FBS, GIBCO) and 1% penicillin/streptomycin (GIBCO) at 37 °C with 5% CO 2 .

Techniques: Two Tailed Test, Virus, Injection, Immunofluorescence, Staining, Western Blot

Clinical information of  ESCC  patients.

Journal: Cancers

Article Title: Drug Repurposing Applications to Overcome Male Predominance via Targeting G2/M Checkpoint in Human Esophageal Squamous Cell Carcinoma

doi: 10.3390/cancers14235854

Figure Lengend Snippet: Clinical information of ESCC patients.

Article Snippet: The human ESCC cell lines KYSE30, KYSE150, KYSE450, and KYSE510 were generously provided by Dr. Yutaka Shimada.

Techniques:

Male ESCC cell lines were more sensitive to decitabine and MK1775 than females. ( a ) Workflow of drug repurposing by using the gene expression data of patients over 60 years old. ( b ) Ten drugs were selected from the drug repurposing results. ( c , d ), Growth curves of KYSE150, KYSE510, KYSE30, and KYSE450 cells were measured by IncuCyte S3 for 72 h. KYSE30 and KYSE450 cells were derived from male patients, while KYSE150 and KYSE510 cells were derived from female patients. Cells were treated with decitabine (10 μM) or MK1775 (200 nM). ( e – g ), Representative image, tumor weights, and tumor volumes of xenografts derived from KYSE30 cells (male), KYSE150 cells (female), and KYSE450 (male) that were treated with decitabine (1.0 mg/kg, i.p.) or MK1775 (60 mg/kg, p.o.). The data shown are the mean ± SD; n = 6 mice per group in KYSE30 and KYSE150; n = 5 mice per group in 450. For tumor weights, data were analyzed using two-tailed t-tests; for tumor volumes, data were analyzed using two-way ANOVA with Bonferroni correction. (* p < 0.05, ** p < 0.01, and *** p < 0.001; ns = not significant).

Journal: Cancers

Article Title: Drug Repurposing Applications to Overcome Male Predominance via Targeting G2/M Checkpoint in Human Esophageal Squamous Cell Carcinoma

doi: 10.3390/cancers14235854

Figure Lengend Snippet: Male ESCC cell lines were more sensitive to decitabine and MK1775 than females. ( a ) Workflow of drug repurposing by using the gene expression data of patients over 60 years old. ( b ) Ten drugs were selected from the drug repurposing results. ( c , d ), Growth curves of KYSE150, KYSE510, KYSE30, and KYSE450 cells were measured by IncuCyte S3 for 72 h. KYSE30 and KYSE450 cells were derived from male patients, while KYSE150 and KYSE510 cells were derived from female patients. Cells were treated with decitabine (10 μM) or MK1775 (200 nM). ( e – g ), Representative image, tumor weights, and tumor volumes of xenografts derived from KYSE30 cells (male), KYSE150 cells (female), and KYSE450 (male) that were treated with decitabine (1.0 mg/kg, i.p.) or MK1775 (60 mg/kg, p.o.). The data shown are the mean ± SD; n = 6 mice per group in KYSE30 and KYSE150; n = 5 mice per group in 450. For tumor weights, data were analyzed using two-tailed t-tests; for tumor volumes, data were analyzed using two-way ANOVA with Bonferroni correction. (* p < 0.05, ** p < 0.01, and *** p < 0.001; ns = not significant).

Article Snippet: The human ESCC cell lines KYSE30, KYSE150, KYSE450, and KYSE510 were generously provided by Dr. Yutaka Shimada.

Techniques: Gene Expression, Derivative Assay, Two Tailed Test

Validation RNA-seq proves that MK1775 and decitabine showed a sex-biased treatment response by targeting the G2/M checkpoint. ( a ) Drug-gene network between decitabine and MK1775 and their target genes was assessed in STICH. Gene functional ontology analysis in the ( b ) decitabine KYSE30 cell line, ( c ) MK1775 KYSE30 cell line, and ( d ) MK1775 KYSE150 cell line.

Journal: Cancers

Article Title: Drug Repurposing Applications to Overcome Male Predominance via Targeting G2/M Checkpoint in Human Esophageal Squamous Cell Carcinoma

doi: 10.3390/cancers14235854

Figure Lengend Snippet: Validation RNA-seq proves that MK1775 and decitabine showed a sex-biased treatment response by targeting the G2/M checkpoint. ( a ) Drug-gene network between decitabine and MK1775 and their target genes was assessed in STICH. Gene functional ontology analysis in the ( b ) decitabine KYSE30 cell line, ( c ) MK1775 KYSE30 cell line, and ( d ) MK1775 KYSE150 cell line.

Article Snippet: The human ESCC cell lines KYSE30, KYSE150, KYSE450, and KYSE510 were generously provided by Dr. Yutaka Shimada.

Techniques: Biomarker Discovery, RNA Sequencing, Functional Assay

Up-regulated LINC00673 is associated with poor prognosis in esophageal squamous cell carcinoma (ESCC) patients. (A) LINC00673 expression levels were evaluated using quantitative PCR (qPCR) in 39 pairs of ESCC tissues and corresponding non-tumor tissues. *** P < 0.001 (unpaired Student’s t test). (B) Receiver operating characteristic (ROC) curve of LINC00673 in 39 ESCC patients. (C–E) Relationships between LINC00673 expression and the differentiation grade, tumor size, and lymph node metastasis, respectively. (F) Kaplan–Meier curves show the survival of ESCC patients, as grouped by the LINC00673 expression levels. * P < 0.05.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: Up-regulated LINC00673 is associated with poor prognosis in esophageal squamous cell carcinoma (ESCC) patients. (A) LINC00673 expression levels were evaluated using quantitative PCR (qPCR) in 39 pairs of ESCC tissues and corresponding non-tumor tissues. *** P < 0.001 (unpaired Student’s t test). (B) Receiver operating characteristic (ROC) curve of LINC00673 in 39 ESCC patients. (C–E) Relationships between LINC00673 expression and the differentiation grade, tumor size, and lymph node metastasis, respectively. (F) Kaplan–Meier curves show the survival of ESCC patients, as grouped by the LINC00673 expression levels. * P < 0.05.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques: Expressing, Real-time Polymerase Chain Reaction

LINC00673 knockdown suppresses the proliferation of esophageal squamous cell carcinoma (ESCC) cells in vitro . (A) Cell proliferation was assessed by the CCK8 method in KYSE30 and KYSE510 cells. Bars show the mean ± SD of OD 450 from triplicate samples. (B) Cell proliferation was assessed using a colony forming assay. Bar plots show the average number of colonies (±SD) from triplicate samples. * P < 0.05.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: LINC00673 knockdown suppresses the proliferation of esophageal squamous cell carcinoma (ESCC) cells in vitro . (A) Cell proliferation was assessed by the CCK8 method in KYSE30 and KYSE510 cells. Bars show the mean ± SD of OD 450 from triplicate samples. (B) Cell proliferation was assessed using a colony forming assay. Bar plots show the average number of colonies (±SD) from triplicate samples. * P < 0.05.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques: Knockdown, In Vitro

LINC00673 knockdown inhibits esophageal squamous cell carcinoma (ESCC) cell proliferation in vivo . (A,B) Stable KYSE30-shLINC00673 and KYSE510-shLINC00673 cells were injected subcutaneously into nude mice. After 4 weeks, the tumors were resected. (C) Tumor growth was measured by Vernier calipers every 3 days starting on the fourth day after injection. Line chart show the tumor growth curve. (D) Box plot showing the tumor weights of the control and LINC00673 knockdown groups. * P < 0.05, *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: LINC00673 knockdown inhibits esophageal squamous cell carcinoma (ESCC) cell proliferation in vivo . (A,B) Stable KYSE30-shLINC00673 and KYSE510-shLINC00673 cells were injected subcutaneously into nude mice. After 4 weeks, the tumors were resected. (C) Tumor growth was measured by Vernier calipers every 3 days starting on the fourth day after injection. Line chart show the tumor growth curve. (D) Box plot showing the tumor weights of the control and LINC00673 knockdown groups. * P < 0.05, *** P < 0.001.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques: Knockdown, In Vivo, Injection, Control

LINC00673 knockdown arrests the cell cycle at the G1/S checkpoint in esophageal squamous cell carcinoma (ESCC) cells. (A,B) Cell cycle examined by a flow cytometry assay. Bar plots show the proportion of cells in the G1 phase, S phase, and G2 phase. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: LINC00673 knockdown arrests the cell cycle at the G1/S checkpoint in esophageal squamous cell carcinoma (ESCC) cells. (A,B) Cell cycle examined by a flow cytometry assay. Bar plots show the proportion of cells in the G1 phase, S phase, and G2 phase. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques: Knockdown, Flow Cytometry

LINC00673 knockdown improved CDKN2C levels in esophageal squamous cell carcinoma (ESCC) cells. (A,C) The levels of the G1/S checkpoint regulator expression were detected by Western blotting analysis in stable KYSE30-shLINC00673, KYSE510-shLINC00673, and corresponding control cells. (B,D) Bar plots showing the relative expression levels of the G1/S checkpoint associated regulators. The image was processed by ImageJ software. * P < 0.05, ** P < 0.01.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: LINC00673 knockdown improved CDKN2C levels in esophageal squamous cell carcinoma (ESCC) cells. (A,C) The levels of the G1/S checkpoint regulator expression were detected by Western blotting analysis in stable KYSE30-shLINC00673, KYSE510-shLINC00673, and corresponding control cells. (B,D) Bar plots showing the relative expression levels of the G1/S checkpoint associated regulators. The image was processed by ImageJ software. * P < 0.05, ** P < 0.01.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques: Knockdown, Expressing, Western Blot, Control, Software

Schematic of the regulatory relationships among LINC00673, EZH2, and CDKN2C in ESCC cells. (A,B) Illustrated the effect of up-regulated or down-regulated LINC00673 on ESCC cell proliferation, respectively.

Journal: Frontiers in Oncology

Article Title: LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation

doi: 10.3389/fonc.2020.01546

Figure Lengend Snippet: Schematic of the regulatory relationships among LINC00673, EZH2, and CDKN2C in ESCC cells. (A,B) Illustrated the effect of up-regulated or down-regulated LINC00673 on ESCC cell proliferation, respectively.

Article Snippet: The human ESCC cell lines (KYSE30, KYSE510, and EC9706) were purchased from Guangdong Hybribio Biotech Ltd. (Guangdong, China), and an immortalized normal esophageal epithelial cell line (HET-1A) was purchased from Cinoasia Institute (Shanghai, China).

Techniques:

Dihydrotanshinone I inhibits proliferation of esophageal squamous cell carcinoma cells while showing no proliferation inhibition in normal esophageal epithelial cells. A-E: Cell viability of esophageal squamous cell carcinoma cells (KYSE30, Eca109, KYSE-450, and KYSE-510) and normal esophageal epithelial cells (Het-1A) after treatment with dihydrotanshinone I for 12 h, 24 h, and 36 h. DHTS: Dihydrotanshinone I.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I inhibits proliferation of esophageal squamous cell carcinoma cells while showing no proliferation inhibition in normal esophageal epithelial cells. A-E: Cell viability of esophageal squamous cell carcinoma cells (KYSE30, Eca109, KYSE-450, and KYSE-510) and normal esophageal epithelial cells (Het-1A) after treatment with dihydrotanshinone I for 12 h, 24 h, and 36 h. DHTS: Dihydrotanshinone I.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Inhibition

Dihydrotanshinone I induces cell cycle arrest in the G0/1 phase in esophageal squamous cell carcinoma cells. A and B: Cell cycle distribution after treatment with DHTS for 24 h in KYSE30 cells and Eca109 cells; C and D: Western blot analysis of proteins associated with the cell cycle in KYSE30 cells and Eca109 cells. a P < 0.05 vs control. DHTS: Dihydrotanshinone I.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I induces cell cycle arrest in the G0/1 phase in esophageal squamous cell carcinoma cells. A and B: Cell cycle distribution after treatment with DHTS for 24 h in KYSE30 cells and Eca109 cells; C and D: Western blot analysis of proteins associated with the cell cycle in KYSE30 cells and Eca109 cells. a P < 0.05 vs control. DHTS: Dihydrotanshinone I.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Western Blot, Control

Dihydrotanshinone I induces apoptosis in esophageal squamous cell carcinoma cells. A and B: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in KYSE30 cells and Eca109 cells; C and D: Apoptosis-related morphologic changes in the cells detected using Hoechst 33258 staining in KYSE30 cells and Eca109 cells. a P < 0.05 vs control.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I induces apoptosis in esophageal squamous cell carcinoma cells. A and B: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in KYSE30 cells and Eca109 cells; C and D: Apoptosis-related morphologic changes in the cells detected using Hoechst 33258 staining in KYSE30 cells and Eca109 cells. a P < 0.05 vs control.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Flow Cytometry, Double Staining, Staining, Control

Dihydrotanshinone I activates the mitochondrial pathway in esophageal squamous cell carcinoma cells. A and B: Bax and Bcl2 levels detected using Western blot and the ratio of Bax and Bcl2 calculated in KYSE30 cells and Eca109 cells; C and D: Proteins associated with the mitochondrial pathway detected using Western blot in KYSE30 cells and Eca109 cells. a P < 0.05 vs control.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I activates the mitochondrial pathway in esophageal squamous cell carcinoma cells. A and B: Bax and Bcl2 levels detected using Western blot and the ratio of Bax and Bcl2 calculated in KYSE30 cells and Eca109 cells; C and D: Proteins associated with the mitochondrial pathway detected using Western blot in KYSE30 cells and Eca109 cells. a P < 0.05 vs control.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Western Blot, Control

Dihydrotanshinone I inhibits the expression of phosphorylated STAT3 in esophageal squamous cell carcinoma cells. A and B: Levels of STAT3 and pSTAT3 detected using Western blot in KYSE30 cells and Eca109 cells; C and D: Expression and location of phosphorylated STAT3 detected by immunofluorescence in KYSE30 cells and Eca109 cells. pSTAT3: Phosphorylated STAT3.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I inhibits the expression of phosphorylated STAT3 in esophageal squamous cell carcinoma cells. A and B: Levels of STAT3 and pSTAT3 detected using Western blot in KYSE30 cells and Eca109 cells; C and D: Expression and location of phosphorylated STAT3 detected by immunofluorescence in KYSE30 cells and Eca109 cells. pSTAT3: Phosphorylated STAT3.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Expressing, Western Blot, Immunofluorescence

STAT3 knockdown promotes dihydrotanshinone I-induced apoptosis in esophageal squamous cell carcinoma cells. A: Knockdown efficiency of STAT3 and phosphorylated STAT3 identified using Western blot in esophageal squamous cell carcinoma cells; B and C: Knockdown efficiency of STAT3 identified using RT-qPCR in KYSE30 cells and Eca109 cells; D: Apoptosis-related morphological changes in STAT3 knockdown cells detected using Hoechst 33258 staining in KYSE30/sh-vector and KYSE30/shSTAT3 cells treated with 0.5 μmol/L DHTS; E: Apoptosis-related morphologic changes detected using Hoechst 33258 staining in Eca109/sh-vector and Eca109/shSTAT3 cells treated with 5 μmol/L DHTS; F: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in KYSE30/sh-vector and KYSE30/shSTAT3 cells treated with 0.5 μmol/L DHTS; G: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in Eca109/sh-vector and Eca109/shSTAT3 cells treated with 5 μmol/L. a P < 0.05.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: STAT3 knockdown promotes dihydrotanshinone I-induced apoptosis in esophageal squamous cell carcinoma cells. A: Knockdown efficiency of STAT3 and phosphorylated STAT3 identified using Western blot in esophageal squamous cell carcinoma cells; B and C: Knockdown efficiency of STAT3 identified using RT-qPCR in KYSE30 cells and Eca109 cells; D: Apoptosis-related morphological changes in STAT3 knockdown cells detected using Hoechst 33258 staining in KYSE30/sh-vector and KYSE30/shSTAT3 cells treated with 0.5 μmol/L DHTS; E: Apoptosis-related morphologic changes detected using Hoechst 33258 staining in Eca109/sh-vector and Eca109/shSTAT3 cells treated with 5 μmol/L DHTS; F: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in KYSE30/sh-vector and KYSE30/shSTAT3 cells treated with 0.5 μmol/L DHTS; G: Cell apoptosis analyzed using flow cytometry with annexin V-PE/7-ADD double staining in Eca109/sh-vector and Eca109/shSTAT3 cells treated with 5 μmol/L. a P < 0.05.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Knockdown, Western Blot, Quantitative RT-PCR, Staining, Plasmid Preparation, Flow Cytometry, Double Staining

STAT3 knockdown synergizes with dihydrotanshinone I in the activation of the mitochondrial pathway in esophageal squamous cell carcinoma cells. A: KYSE30/sh-vector and KYSE30/shSTAT3 cells were treated with 0.5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins; B: Eca109/sh-vector and Eca109/shSTAT3 cells were treated with 5 μmol/L dihydrotanshinone I, and Western blot was performed to detect the levels of related proteins.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: STAT3 knockdown synergizes with dihydrotanshinone I in the activation of the mitochondrial pathway in esophageal squamous cell carcinoma cells. A: KYSE30/sh-vector and KYSE30/shSTAT3 cells were treated with 0.5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins; B: Eca109/sh-vector and Eca109/shSTAT3 cells were treated with 5 μmol/L dihydrotanshinone I, and Western blot was performed to detect the levels of related proteins.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Knockdown, Activation Assay, Plasmid Preparation, Western Blot

STAT3 overexpression blocks the mitochondrial pathway activated by dihydrotanshinone I in esophageal squamous cell carcinoma cells. A: Overexpression efficiency of STAT3 identified using Western blot in esophageal squamous cell carcinoma cells; B and C: Overexpression efficiency of STAT3 identified using RT-qPCR in KYSE30 cells and Eca109 cells; D: KYSE30/OE-vector and KYSE30/OE-STAT3 cells were treated with 0.5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins; E: Eca109/OE-vector and Eca109/OE-STAT3 cells were treated with 5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins. OE: Overexpression. a P < 0.05 vs control.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: STAT3 overexpression blocks the mitochondrial pathway activated by dihydrotanshinone I in esophageal squamous cell carcinoma cells. A: Overexpression efficiency of STAT3 identified using Western blot in esophageal squamous cell carcinoma cells; B and C: Overexpression efficiency of STAT3 identified using RT-qPCR in KYSE30 cells and Eca109 cells; D: KYSE30/OE-vector and KYSE30/OE-STAT3 cells were treated with 0.5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins; E: Eca109/OE-vector and Eca109/OE-STAT3 cells were treated with 5 μmol/L DHTS, and Western blot was performed to detect the levels of related proteins. OE: Overexpression. a P < 0.05 vs control.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: Over Expression, Western Blot, Quantitative RT-PCR, Plasmid Preparation, Control

Dihydrotanshinone I inhibits proliferation and induces apoptosis in esophageal squamous cell carcinoma in vivo . A: Morphology of the subcutaneous implanted tumors; B: Mean tumor volume at each time point; C: Tumor weight obtained at the end of the experiment; D: Recorded body weight of the mice; E: Immunohistochemistry detection of the expression of Ki67 in the tumor tissue; F and G : A TUNEL assay was performed to detect apoptotic cells in the tumor tissue. a P < 0.05 vs control.

Journal: World Journal of Gastrointestinal Oncology

Article Title: STAT3-mediated activation of mitochondrial pathway contributes to antitumor effect of dihydrotanshinone I in esophageal squamous cell carcinoma cells

doi: 10.4251/wjgo.v13.i8.893

Figure Lengend Snippet: Dihydrotanshinone I inhibits proliferation and induces apoptosis in esophageal squamous cell carcinoma in vivo . A: Morphology of the subcutaneous implanted tumors; B: Mean tumor volume at each time point; C: Tumor weight obtained at the end of the experiment; D: Recorded body weight of the mice; E: Immunohistochemistry detection of the expression of Ki67 in the tumor tissue; F and G : A TUNEL assay was performed to detect apoptotic cells in the tumor tissue. a P < 0.05 vs control.

Article Snippet: The human ESCC cell lines KYSE30, Eca109, KYSE450, and KYSE510 and human normal esophageal epithelial cell line Het-1A were donated by the China Center for Type Culture Collection.

Techniques: In Vivo, Immunohistochemistry, Expressing, TUNEL Assay, Control

PRDX4 exhibits high expression in ESCC tissues and cells. (A) Sangerbox 3.0 online software assay for PRDX4 expression in pan-cancer. (B) UALCAN database investigation for PRDX4 expression in ESCA samples and normal esophageal epithelial tissues. (C) GEO dataset GSE111011 was used to investigate the expression of PRDX4 in ESCC samples and paired normal samples. (D) RT-qPCR assay was used to assess the expression of PRDX4 in 65 ESCC samples and paired normal samples. (E) Western blot analysis of the protein expression of PRDX4 in eight ESCC samples and paired normal samples. (F) The relative protein levels of PRDX4 in eight ESCC samples and paired normal samples. (G) IHC detection of PRDX4 expression in normal tissues and ESCC tissues. Scale bar, 20 µm. (H) Western blot analysis of PRDX4 protein expression in ESCC cell lines (KYSE70, KYSE450, KYSE520, KYSE30 and KYSE270) and normal esophageal epithelial cell line Het-1A. (I) The relative protein levels of PRDX4 in ESCC cell lines and Het-1A cells. (J) RT-qPCR assay of PRDX4 mRNA expression in the aforementioned ESCC cell lines and Het-1A cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; ns, not significant.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: PRDX4 exhibits high expression in ESCC tissues and cells. (A) Sangerbox 3.0 online software assay for PRDX4 expression in pan-cancer. (B) UALCAN database investigation for PRDX4 expression in ESCA samples and normal esophageal epithelial tissues. (C) GEO dataset GSE111011 was used to investigate the expression of PRDX4 in ESCC samples and paired normal samples. (D) RT-qPCR assay was used to assess the expression of PRDX4 in 65 ESCC samples and paired normal samples. (E) Western blot analysis of the protein expression of PRDX4 in eight ESCC samples and paired normal samples. (F) The relative protein levels of PRDX4 in eight ESCC samples and paired normal samples. (G) IHC detection of PRDX4 expression in normal tissues and ESCC tissues. Scale bar, 20 µm. (H) Western blot analysis of PRDX4 protein expression in ESCC cell lines (KYSE70, KYSE450, KYSE520, KYSE30 and KYSE270) and normal esophageal epithelial cell line Het-1A. (I) The relative protein levels of PRDX4 in ESCC cell lines and Het-1A cells. (J) RT-qPCR assay of PRDX4 mRNA expression in the aforementioned ESCC cell lines and Het-1A cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; ns, not significant.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Expressing, Software, Quantitative RT-PCR, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Gene Expression, Immunohistochemistry

High expression of PRDX4 predicts a poor prognosis in patients with ESCC (A) UALCAN assay of the effects of PRDX4 expression on the survival of patients with ESCA. (B) GEPIA online software assay of the effects of PRDX4 expression on the survival of patients with ESCA. (C) Sangerbox 3.0 online software assay identifying high PRDX4 expression as a poor prognostic factor in patients with ESCA. (D) RT-qPCR assay for PRDX4 expression in patients with ESCC with different TNM stages. (E) RT-qPCR assay of PRDX4 expression in patients with ESCC without lymph node metastasis and with lymph node metastasis. (F) Log-rank test determination of the prognostic value of PRDX4 in patients with ESCC. ** P<0.01 and *** P<0.001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; GEPIA, Gene Expression Profiling Interactive Analysis; RT-qPCR, reverse transcription quantitative polymerase chain reaction; TNM, tumor-node-metastasis.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: High expression of PRDX4 predicts a poor prognosis in patients with ESCC (A) UALCAN assay of the effects of PRDX4 expression on the survival of patients with ESCA. (B) GEPIA online software assay of the effects of PRDX4 expression on the survival of patients with ESCA. (C) Sangerbox 3.0 online software assay identifying high PRDX4 expression as a poor prognostic factor in patients with ESCA. (D) RT-qPCR assay for PRDX4 expression in patients with ESCC with different TNM stages. (E) RT-qPCR assay of PRDX4 expression in patients with ESCC without lymph node metastasis and with lymph node metastasis. (F) Log-rank test determination of the prognostic value of PRDX4 in patients with ESCC. ** P<0.01 and *** P<0.001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; ESCA, esophageal carcinoma; GEPIA, Gene Expression Profiling Interactive Analysis; RT-qPCR, reverse transcription quantitative polymerase chain reaction; TNM, tumor-node-metastasis.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Expressing, Software, Quantitative RT-PCR, Gene Expression, Reverse Transcription, Real-time Polymerase Chain Reaction

PRDX4 knockdown suppresses cell proliferation in ESCC cells. (A) Western blot analysis of the protein expression of PRDX4 in KYSE270 cells transfected with PRDX4 siRNA and KYSE30 cells transfected with pcDNA3.1-PRDX4. (B) The relative protein levels of PRDX4 in KYSE270 and KYSE30 cells with different transfections. (C) RT-qPCR assay of the mRNA expression of PRDX4 in KYSE270 cells transfected with PRDX4 siRNA and KYSE30 cells transfected with pcDNA3.1-PRDX4. (D) CCK-8 assay of cell proliferation in KYSE270 cells transfected with PRDX4 siRNA. (E) Colony formation assay of the colony-forming ability of KYSE270 cells transfected with PRDX4 siRNA. (F) Statistical analysis of the number of colonies formed in KYSE270 cells transfected with PRDX4 siRNA. (G) CCK-8 assay of cell proliferation in KYSE30 cells transfected with pcDNA3.1-PRDX4. (H) Colony formation assay of the colony-forming ability of KYSE30 cells transfected with pcDNA3.1-PRDX4. (I) Statistical analysis of the number of colonies formed in KYSE30 cells transfected with pcDNA3.1-PRDX4. (J) EdU staining assay of EdU-positive cells in KYSE270 cells transfected with PRDX4 siRNA. Scale bar, 100 µm. (K) EdU staining assay of EdU-positive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. Scale bar, 100 µm. (L) Statistical analysis of the number of EdU-positive cells in KYSE270 cells transfected with PRDX4 siRNA. (M) Statistical analysis of the number of EdU-positive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; CCK-8, Cell Counting Kit-8; EdU, 5-ethynyl-2'-deoxyuridine.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: PRDX4 knockdown suppresses cell proliferation in ESCC cells. (A) Western blot analysis of the protein expression of PRDX4 in KYSE270 cells transfected with PRDX4 siRNA and KYSE30 cells transfected with pcDNA3.1-PRDX4. (B) The relative protein levels of PRDX4 in KYSE270 and KYSE30 cells with different transfections. (C) RT-qPCR assay of the mRNA expression of PRDX4 in KYSE270 cells transfected with PRDX4 siRNA and KYSE30 cells transfected with pcDNA3.1-PRDX4. (D) CCK-8 assay of cell proliferation in KYSE270 cells transfected with PRDX4 siRNA. (E) Colony formation assay of the colony-forming ability of KYSE270 cells transfected with PRDX4 siRNA. (F) Statistical analysis of the number of colonies formed in KYSE270 cells transfected with PRDX4 siRNA. (G) CCK-8 assay of cell proliferation in KYSE30 cells transfected with pcDNA3.1-PRDX4. (H) Colony formation assay of the colony-forming ability of KYSE30 cells transfected with pcDNA3.1-PRDX4. (I) Statistical analysis of the number of colonies formed in KYSE30 cells transfected with pcDNA3.1-PRDX4. (J) EdU staining assay of EdU-positive cells in KYSE270 cells transfected with PRDX4 siRNA. Scale bar, 100 µm. (K) EdU staining assay of EdU-positive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. Scale bar, 100 µm. (L) Statistical analysis of the number of EdU-positive cells in KYSE270 cells transfected with PRDX4 siRNA. (M) Statistical analysis of the number of EdU-positive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; CCK-8, Cell Counting Kit-8; EdU, 5-ethynyl-2'-deoxyuridine.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Knockdown, Western Blot, Expressing, Transfection, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Staining, Small Interfering RNA, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Counting

PRDX4 downregulation suppresses cell migration and invasion in ESCC cells. (A) PRDX4 knockdown suppresses cell migration and invasion in KYSE270 cells after transfection with PRDX4 siRNA. Scale bar, 100 µm. (B) Statistical analysis of the number of migratory cells in KYSE270 cells transfected with PRDX4 siRNA. (C) Statistical analysis of the number of invasive cells in KYSE270 cells transfected with PRDX4 siRNA. (D) Western blot analysis of the expression levels of E-cadherin, N-cadherin and vimentin in KYSE270 cells transfected with PRDX4 siRNA. (E) The relative protein levels of E-cadherin, N-cadherin and vimentin in KYSE270 cells transfected with PRDX4 siRNA. (F) PRDX4 overexpression suppresses cell migration and invasion in KYSE30 cells after transfection with pcDNA3.1-PRDX4. Scale bar, 100 µm. (G) Statistical analysis of the number of migratory cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. (H) Statistical analysis of the number of invasive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. (I) Western blot analysis of the expression levels of E-cadherin, N-cadherin and vimentin in KYSE30 cells transfected with pcDNA3.1-PRDX4. (J) The relative protein levels of E-cadherin, N-cadherin and vimentin in KYSE30 cells transfected with pcDNA3.1-PRDX4. *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: PRDX4 downregulation suppresses cell migration and invasion in ESCC cells. (A) PRDX4 knockdown suppresses cell migration and invasion in KYSE270 cells after transfection with PRDX4 siRNA. Scale bar, 100 µm. (B) Statistical analysis of the number of migratory cells in KYSE270 cells transfected with PRDX4 siRNA. (C) Statistical analysis of the number of invasive cells in KYSE270 cells transfected with PRDX4 siRNA. (D) Western blot analysis of the expression levels of E-cadherin, N-cadherin and vimentin in KYSE270 cells transfected with PRDX4 siRNA. (E) The relative protein levels of E-cadherin, N-cadherin and vimentin in KYSE270 cells transfected with PRDX4 siRNA. (F) PRDX4 overexpression suppresses cell migration and invasion in KYSE30 cells after transfection with pcDNA3.1-PRDX4. Scale bar, 100 µm. (G) Statistical analysis of the number of migratory cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. (H) Statistical analysis of the number of invasive cells in KYSE30 cells transfected with pcDNA3.1-PRDX4. (I) Western blot analysis of the expression levels of E-cadherin, N-cadherin and vimentin in KYSE30 cells transfected with pcDNA3.1-PRDX4. (J) The relative protein levels of E-cadherin, N-cadherin and vimentin in KYSE30 cells transfected with pcDNA3.1-PRDX4. *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Migration, Knockdown, Transfection, Western Blot, Expressing, Over Expression, Small Interfering RNA

PRDX4 is an important regulator of ferroptosis in ESCC cells. (A) Determination of MDA, LPO and GSH contents in KYSE270 cells after transfection with PRDX4 siRNA. (B) Western blot analysis of the protein levels of GPX4, SLC7A11 and PTGS2 in KYSE270 cells transfected with PRDX4 siRNA. (C) The relative protein levels of GPX4, SLC7A11 and PTGS2 in KYSE270 cells transfected with PRDX4 siRNA. (D) Determination of MDA, LPO and GSH contents in KYSE30 cells after transfection with pcDNA3.1-PRDX4. (E) Western blot analysis of the protein levels of GPX4, SLC7A11 and PTGS2 in KYSE30 cells transfected with pcDNA3.1-PRDX4. (F) The relative protein levels of GPX4, SLC7A11 and PTGS2 in KYSE30 cells transfected with pcDNA3.1-PRDX4. (G) Detection of the levels of MDA, LPO and GSH in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (H) Western blot analysis of the protein expression levels of GPX4, SLC7A11 and PTGS2 in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (I) The relative protein levels of GPX4, SLC7A11 and PTGS2 in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (J) Detection of the levels of MDA, LPO and GSH in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. (K) Western blot analysis of the protein expression levels of GPX4, SLC7A11 and PTGS2 in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. (L) The relative protein levels of GPX4, SLC7A11 and PTGS2 in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA; MDA, malondialdehyde; LPO, lipid peroxidation; GSH, glutathione; GPX4, glutathione peroxidase 4; SLC7A11, solute carrier family 7 member 11; PTGS2, prostaglandin-endoperoxide synthase 2; Fer-1, ferrostatin-1; ns, not significant.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: PRDX4 is an important regulator of ferroptosis in ESCC cells. (A) Determination of MDA, LPO and GSH contents in KYSE270 cells after transfection with PRDX4 siRNA. (B) Western blot analysis of the protein levels of GPX4, SLC7A11 and PTGS2 in KYSE270 cells transfected with PRDX4 siRNA. (C) The relative protein levels of GPX4, SLC7A11 and PTGS2 in KYSE270 cells transfected with PRDX4 siRNA. (D) Determination of MDA, LPO and GSH contents in KYSE30 cells after transfection with pcDNA3.1-PRDX4. (E) Western blot analysis of the protein levels of GPX4, SLC7A11 and PTGS2 in KYSE30 cells transfected with pcDNA3.1-PRDX4. (F) The relative protein levels of GPX4, SLC7A11 and PTGS2 in KYSE30 cells transfected with pcDNA3.1-PRDX4. (G) Detection of the levels of MDA, LPO and GSH in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (H) Western blot analysis of the protein expression levels of GPX4, SLC7A11 and PTGS2 in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (I) The relative protein levels of GPX4, SLC7A11 and PTGS2 in the control group, PRDX4 siRNA group and PRDX4 siRNA plus Fer-1 group in KYSE270 cells. (J) Detection of the levels of MDA, LPO and GSH in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. (K) Western blot analysis of the protein expression levels of GPX4, SLC7A11 and PTGS2 in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. (L) The relative protein levels of GPX4, SLC7A11 and PTGS2 in the pcDNA3.1 group, pcDNA3.1-PRDX4 group and pcDNA3.1-PRDX4 plus erastin group in KYSE30 cells. ** P<0.01, *** P<0.001 and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA; MDA, malondialdehyde; LPO, lipid peroxidation; GSH, glutathione; GPX4, glutathione peroxidase 4; SLC7A11, solute carrier family 7 member 11; PTGS2, prostaglandin-endoperoxide synthase 2; Fer-1, ferrostatin-1; ns, not significant.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Transfection, Western Blot, Control, Expressing, Small Interfering RNA

PRDX4 suppresses ferroptosis of ESCC cells by activating the PI3K/AKT signaling pathway. (A) Determination of MDA, LPO and GSH contents in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (B) Western blot analysis of the protein expression levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (C) The relative protein levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (D) Detection of MDA, LPO and GSH contents in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. (E) Western blot analysis of the protein expression levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. (F) The relative protein levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. * P<0.05, ** P<0.01, and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; MDA, malondialdehyde; LPO, lipid peroxidation; GSH, glutathione; GPX4, glutathione peroxidase 4; p-PI3K, phosphorylated PI3K; p-AKT, phosphorylated AKT; ns, not significant.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: PRDX4 suppresses ferroptosis of ESCC cells by activating the PI3K/AKT signaling pathway. (A) Determination of MDA, LPO and GSH contents in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (B) Western blot analysis of the protein expression levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (C) The relative protein levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K activator 740 Y-P after PRDX4 knockdown in KYSE270 cells. (D) Detection of MDA, LPO and GSH contents in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. (E) Western blot analysis of the protein expression levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. (F) The relative protein levels of GPX4, p-PI3K, PI3K, p-AKT and AKT in the absence or presence of the PI3K inhibitor LY294002 after PRDX4 overexpression in KYSE30 cells. * P<0.05, ** P<0.01, and **** P<0.0001, indicate statistical significance. PRDX4, peroxiredoxin 4; ESCC, esophageal squamous cell carcinoma; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; MDA, malondialdehyde; LPO, lipid peroxidation; GSH, glutathione; GPX4, glutathione peroxidase 4; p-PI3K, phosphorylated PI3K; p-AKT, phosphorylated AKT; ns, not significant.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Knockdown, Western Blot, Expressing, Over Expression

Proposed model of PRDX4-mediated suppression of ferroptosis through regulation of the PI3K/AKT pathway in ESCC. PRDX4 is highly expressed in ESCC samples and cells. High PRDX4 expression is strongly associated with TNM staging and lymph node metastasis in patients with ESCC and may serve as an indicator of prognosis for patients with ESCA. PRDX4 knockdown suppresses cell proliferation and invasion of ESCC cells by inactivating the PI3K/AKT signaling pathway, thereby triggering ferroptosis in these cells. PRDX4, peroxiredoxin 4; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; ESCC, esophageal squamous cell carcinoma; TNM, tumor-node-metastasis; ESCA, esophageal carcinoma.

Journal: Biomedical Reports

Article Title: Peroxiredoxin 4 suppresses ferroptosis in esophageal squamous cell carcinoma by activating the phosphoinositide 3-kinase  signaling pathway

doi: 10.3892/br.2026.2133

Figure Lengend Snippet: Proposed model of PRDX4-mediated suppression of ferroptosis through regulation of the PI3K/AKT pathway in ESCC. PRDX4 is highly expressed in ESCC samples and cells. High PRDX4 expression is strongly associated with TNM staging and lymph node metastasis in patients with ESCC and may serve as an indicator of prognosis for patients with ESCA. PRDX4 knockdown suppresses cell proliferation and invasion of ESCC cells by inactivating the PI3K/AKT signaling pathway, thereby triggering ferroptosis in these cells. PRDX4, peroxiredoxin 4; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; ESCC, esophageal squamous cell carcinoma; TNM, tumor-node-metastasis; ESCA, esophageal carcinoma.

Article Snippet: The human ESCC cell line KYSE30 was purchased from Procell Life Science &Technology Co., Ltd. Normal esophageal epithelial cell line Het-1A and human ESCC cell lines KYSE520, KYSE70, KYSE450, and KYSE270, which were authenticated by STR profiling, were purchased from Qingqi Shanghai Biotechnology Development Co., Ltd. ESCC cells were cultured in RPMI-1640 medium (Procell Life Science & Technology Co., Ltd.) supplemented with 10% fetal bovine serum (FBS; Suzhou ShuangRu Biotech Co., Ltd.), as well as penicillin (100 U/ml) and streptomycin (0.1 mg/ml) solution (Solarbio Life Sciences), and were incubated at 37 ̊C with 5% CO 2 .

Techniques: Expressing, Knockdown

The expression of BAALC‐AS1 in ESCC. A. In situ hybridization of BALC‐AS1 in ESCC tissue samples and their corresponding adjacent normal tissues. Scale bar: left, 100 μm; right, 200 μm. Adjacent, adjacent normal tissues; Cancer, ESCC tissues. B. Comparison of BAALC‐AS1 scores of ESCC and adjacent normal tissues. C. ESCC patients with high levels of BAALC‐AS1 expression showed reduced survival compared with those with low levels of BAALC‐AS1 expression ( P = 0.037; log‐rank test). D. Differences in the overall survival and pathological stage between patients with high BAALC‐AS1 expression level and low BAALC‐AS1 expression level were highly significant. E. Expression of BAALC‐AS1 quantified by RT‐qPCR in ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510, and COLO‐680) and normal esophageal epithelial cell line (Het‐1A). F. Analysis of BAALC‐AS1 distribution by cellular fractionation followed RT‐qPCR in KYSE‐510 cells. U6 and 18s mRNAs were served as controls for nuclear and cytoplasmic RNAs, respectively. G. RNA‐ FISH was performed to detect BAALC‐AS1 expression in KYSE‐510 cells. The nuclei were counterstained with 4′,6‐diamidino‐2‐phenylindole (DAPI). Scale bar, 10 μm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. All of the values are expressed as the mean ± SEM of 3 experiments

Journal: Cancer Communications

Article Title: BAALC‐AS1/G3BP2/c‐Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma

doi: 10.1002/cac2.12127

Figure Lengend Snippet: The expression of BAALC‐AS1 in ESCC. A. In situ hybridization of BALC‐AS1 in ESCC tissue samples and their corresponding adjacent normal tissues. Scale bar: left, 100 μm; right, 200 μm. Adjacent, adjacent normal tissues; Cancer, ESCC tissues. B. Comparison of BAALC‐AS1 scores of ESCC and adjacent normal tissues. C. ESCC patients with high levels of BAALC‐AS1 expression showed reduced survival compared with those with low levels of BAALC‐AS1 expression ( P = 0.037; log‐rank test). D. Differences in the overall survival and pathological stage between patients with high BAALC‐AS1 expression level and low BAALC‐AS1 expression level were highly significant. E. Expression of BAALC‐AS1 quantified by RT‐qPCR in ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510, and COLO‐680) and normal esophageal epithelial cell line (Het‐1A). F. Analysis of BAALC‐AS1 distribution by cellular fractionation followed RT‐qPCR in KYSE‐510 cells. U6 and 18s mRNAs were served as controls for nuclear and cytoplasmic RNAs, respectively. G. RNA‐ FISH was performed to detect BAALC‐AS1 expression in KYSE‐510 cells. The nuclei were counterstained with 4′,6‐diamidino‐2‐phenylindole (DAPI). Scale bar, 10 μm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. All of the values are expressed as the mean ± SEM of 3 experiments

Article Snippet: The normal esophageal epithelial cell line (Het‐1A) and the human ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510 and COLO‐680) were generously provided by Dr. Yutaka Shimada of Kyoto University (Kyoto, Japan) and cultured as previously described [ ].

Techniques: Expressing, In Situ Hybridization, Comparison, Quantitative RT-PCR, Cell Fractionation

BAALC‐AS1 promotes tumor growth of ESCC in vivo . A. Images of the xenograft tumors formed in nude mice injected with BAALC‐AS1‐overexpressing (BAALC‐AS1) or ‐silencing (sh/BAALC‐AS1‐1 and ‐2) KYSE‐450 or KYSE‐410 cells. The nude mice injected with control cells (Vector and siNC) were used as control. B. Tumor weight in nude mice injected with the abovementioned cells. C. Growth curve of xenograft tumors in nude mice injected with the abovementioned cells. Five mice per group were used in the tumor formation assay. D. The body weight of the nude mice in tumor formation assay. E. Representative images of H&E staining and Ki67 IHC staining for tumor tissues harvested from nude mice in tumor formation assay. Scale bar, 50 μm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. All values are expressed as the mean ± SEM

Journal: Cancer Communications

Article Title: BAALC‐AS1/G3BP2/c‐Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma

doi: 10.1002/cac2.12127

Figure Lengend Snippet: BAALC‐AS1 promotes tumor growth of ESCC in vivo . A. Images of the xenograft tumors formed in nude mice injected with BAALC‐AS1‐overexpressing (BAALC‐AS1) or ‐silencing (sh/BAALC‐AS1‐1 and ‐2) KYSE‐450 or KYSE‐410 cells. The nude mice injected with control cells (Vector and siNC) were used as control. B. Tumor weight in nude mice injected with the abovementioned cells. C. Growth curve of xenograft tumors in nude mice injected with the abovementioned cells. Five mice per group were used in the tumor formation assay. D. The body weight of the nude mice in tumor formation assay. E. Representative images of H&E staining and Ki67 IHC staining for tumor tissues harvested from nude mice in tumor formation assay. Scale bar, 50 μm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. All values are expressed as the mean ± SEM

Article Snippet: The normal esophageal epithelial cell line (Het‐1A) and the human ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510 and COLO‐680) were generously provided by Dr. Yutaka Shimada of Kyoto University (Kyoto, Japan) and cultured as previously described [ ].

Techniques: In Vivo, Injection, Control, Plasmid Preparation, Tube Formation Assay, Staining, Immunohistochemistry

c‐Myc acts directly with the BAALC‐AS1 promoter. A. Expression of BAALC‐AS1 quantified by RT‐qPCR after c‐Myc knockdown in KYSE‐450 cells. B. Silencing c‐Myc decreased the luciferase activity controlled by BAALC‐AS1 promoter. C. Summary diagram describing how BAALC‐AS1 regulates proliferation in ESCC cells. NC, negative control; si/c‐Myc, small interfering RNA for c‐Myc; *, P < 0.05. All values are expressed as the mean ± SEM of 3 experiments

Journal: Cancer Communications

Article Title: BAALC‐AS1/G3BP2/c‐Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma

doi: 10.1002/cac2.12127

Figure Lengend Snippet: c‐Myc acts directly with the BAALC‐AS1 promoter. A. Expression of BAALC‐AS1 quantified by RT‐qPCR after c‐Myc knockdown in KYSE‐450 cells. B. Silencing c‐Myc decreased the luciferase activity controlled by BAALC‐AS1 promoter. C. Summary diagram describing how BAALC‐AS1 regulates proliferation in ESCC cells. NC, negative control; si/c‐Myc, small interfering RNA for c‐Myc; *, P < 0.05. All values are expressed as the mean ± SEM of 3 experiments

Article Snippet: The normal esophageal epithelial cell line (Het‐1A) and the human ESCC cell lines (YES‐2, KYSE‐30, ‐150, ‐180, ‐410, ‐450, ‐510 and COLO‐680) were generously provided by Dr. Yutaka Shimada of Kyoto University (Kyoto, Japan) and cultured as previously described [ ].

Techniques: Expressing, Quantitative RT-PCR, Knockdown, Luciferase, Activity Assay, Negative Control, Small Interfering RNA

Spatial whole-transcriptome profiling of ESPL and ESCC samples (A) Workflow of DSP experimental process. (B) The UMAP plot displaying the clustering results of AOIs from different compartments at multiple stages of ESCC. (C) The heatmap displaying the expression levels of AOI characteristic markers RNA in different compartments. (D) The boxplots showing the expression levels of marker genes in five different compartments at different stages of ESCC. Box plot shows the median and interquartile range, whiskers extend to 1.5 × IQR. DSP, digital spatial profiling; UMAP, uniform manifold approximation and projection; AOI, area of interest; EP, epithelial-cell-enriched; MC, macrophage-cell-enriched; NC, neutrophil-cell-enriched; ST, stroma-enriched; LS, lymphoid structure; CAFs, cancer-associated fibroblasts; ESPL, esophageal squamous precancerous lesion; non-mESCC, non-metastasis esophageal squamous cell carcinoma; mESCC, metastasis esophageal squamous cell carcinoma; mLN, lymph node metastasis tissues.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: Spatial whole-transcriptome profiling of ESPL and ESCC samples (A) Workflow of DSP experimental process. (B) The UMAP plot displaying the clustering results of AOIs from different compartments at multiple stages of ESCC. (C) The heatmap displaying the expression levels of AOI characteristic markers RNA in different compartments. (D) The boxplots showing the expression levels of marker genes in five different compartments at different stages of ESCC. Box plot shows the median and interquartile range, whiskers extend to 1.5 × IQR. DSP, digital spatial profiling; UMAP, uniform manifold approximation and projection; AOI, area of interest; EP, epithelial-cell-enriched; MC, macrophage-cell-enriched; NC, neutrophil-cell-enriched; ST, stroma-enriched; LS, lymphoid structure; CAFs, cancer-associated fibroblasts; ESPL, esophageal squamous precancerous lesion; non-mESCC, non-metastasis esophageal squamous cell carcinoma; mESCC, metastasis esophageal squamous cell carcinoma; mLN, lymph node metastasis tissues.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Expressing, Marker

Changes in gene expression patterns in the EP compartment during the initiation of ESCC (A) Volcano plot showed significant DEGs during the formation of ESPL. (B) Pathway enrichment analysis of DEGs in ESPL and normal stages. (C) Changes in gene expression across epidermis development and keratinocyte differentiation pathways during ESPL formation. (D) Interaction plot of ESPL-formation-related genes. Each circle represents a protein, and the interactions are connected by solid lines. The types of interactions were shown on the right side of the figure. (E) The four-quadrant plot illustrates the significant differences in gene expression patterns among four distinct types during the initiation of ESCC. (F) The boxplot shows the expression levels of the presented genes across the four patterns during ESCC initiation. Pattern 1 to 4 were tagged in blue, pink, yellow, and purple, respectively. Box plot shows the interquartile, whiskers extend to1.5 × IQR. (G) Pathway enrichment results for genes in the four patterns. (H) The line graph depicts changes in the signature scores of the indicated pathways during the initiation and development of ESCC. DEGs, differentially expressed genes.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: Changes in gene expression patterns in the EP compartment during the initiation of ESCC (A) Volcano plot showed significant DEGs during the formation of ESPL. (B) Pathway enrichment analysis of DEGs in ESPL and normal stages. (C) Changes in gene expression across epidermis development and keratinocyte differentiation pathways during ESPL formation. (D) Interaction plot of ESPL-formation-related genes. Each circle represents a protein, and the interactions are connected by solid lines. The types of interactions were shown on the right side of the figure. (E) The four-quadrant plot illustrates the significant differences in gene expression patterns among four distinct types during the initiation of ESCC. (F) The boxplot shows the expression levels of the presented genes across the four patterns during ESCC initiation. Pattern 1 to 4 were tagged in blue, pink, yellow, and purple, respectively. Box plot shows the interquartile, whiskers extend to1.5 × IQR. (G) Pathway enrichment results for genes in the four patterns. (H) The line graph depicts changes in the signature scores of the indicated pathways during the initiation and development of ESCC. DEGs, differentially expressed genes.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Gene Expression, Expressing

Spatial transcriptome analysis of the TME during ESCC initiation process (A) Quantitative analysis of immune cells in non-EP compartments during the initiation process of ESCC using TME_consense algorithm. (B) Comparison of B, plasma, CD4 + T, and CD8 + T cells during the initiation process of ESCC. (C) Analyze the immune cell changes in non-EP compartments during the initiation process of ESCC using SpatialDecon algorithm. (D) mIF staining of CD20, CD8, and CD4 on tumor tissues in ESCC initiation stages. Scale bar, 200 μm. (E) Comparison of the percentages of CD20-, CD8-, and CD4-positive cells across the ESCC initiation stages. (F) Pathway enrichment analysis of significantly differential expression genes in non-EP compartments during the initial stage of ESCC. (G) The heatmap shows the differential genes in the MC and NC compartments during the initial stage of ESCC. (H) Comparison of the proportion of tumor-associated macrophage and neutrophile cells across the ESCC development. (I) The heatmap shows the differential genes in TLS compartments during the initial stage of ESCC. (J) mIF staining on TLS compartment of ESCC initiation stage. Scale bar, 100 μm. (K) Comparison of the percentages of APOBEC3A-positive cells between ESPL and non-mESCC stages in the TLS. NE, normal epithelia; ESCC, esophageal squamous cell carcinoma; mIF, multiplex immunofluorescence; MC, macrophage-cell-enriched compartment; NC, neutrophil-cell-enriched compartment; TLS, tertiary lymphoid structures. Box plots show the median and interquartile range, whiskers extend to 1.5×IQR. ∗p < 0.05 , ∗∗ p < 0.01,∗∗∗ p < 0.001, p values were calculated using a two-sided Wilcoxon rank-sum test.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: Spatial transcriptome analysis of the TME during ESCC initiation process (A) Quantitative analysis of immune cells in non-EP compartments during the initiation process of ESCC using TME_consense algorithm. (B) Comparison of B, plasma, CD4 + T, and CD8 + T cells during the initiation process of ESCC. (C) Analyze the immune cell changes in non-EP compartments during the initiation process of ESCC using SpatialDecon algorithm. (D) mIF staining of CD20, CD8, and CD4 on tumor tissues in ESCC initiation stages. Scale bar, 200 μm. (E) Comparison of the percentages of CD20-, CD8-, and CD4-positive cells across the ESCC initiation stages. (F) Pathway enrichment analysis of significantly differential expression genes in non-EP compartments during the initial stage of ESCC. (G) The heatmap shows the differential genes in the MC and NC compartments during the initial stage of ESCC. (H) Comparison of the proportion of tumor-associated macrophage and neutrophile cells across the ESCC development. (I) The heatmap shows the differential genes in TLS compartments during the initial stage of ESCC. (J) mIF staining on TLS compartment of ESCC initiation stage. Scale bar, 100 μm. (K) Comparison of the percentages of APOBEC3A-positive cells between ESPL and non-mESCC stages in the TLS. NE, normal epithelia; ESCC, esophageal squamous cell carcinoma; mIF, multiplex immunofluorescence; MC, macrophage-cell-enriched compartment; NC, neutrophil-cell-enriched compartment; TLS, tertiary lymphoid structures. Box plots show the median and interquartile range, whiskers extend to 1.5×IQR. ∗p < 0.05 , ∗∗ p < 0.01,∗∗∗ p < 0.001, p values were calculated using a two-sided Wilcoxon rank-sum test.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Comparison, Clinical Proteomics, Staining, Quantitative Proteomics, Multiplex Assay, Immunofluorescence

Characteristic changes in transcription patterns during the progression of ESCC (A) The volcano plot shows significant differences in genes between the early (ESPL and non-mESCC) and advanced (mESCC and mLN) stages of ESCC. (B) Pathway enrichment analysis of differentially expressed genes in the early and advanced stages of ESCC. (C) The gene expression levels associated with significantly enriched pathways throughout the occurrence and development of ESCC. (D) mIF staining of CCND1, LAMB1, and IL-18 on ESCC tissues. Scale bar, 200 μm. (E) Comparison of the percentages of CCND1, LAMB1, and IL-18-positive cells on ESCC tissues. Box plots show the median and interquartile range, whiskers extend to 1.5 × IQR. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, p values were calculated using a two-sided Wilcoxon rank-sum test. (F) The heatmap of gradient-changed DEGs based on pseudotime and ESCC progression of EP.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: Characteristic changes in transcription patterns during the progression of ESCC (A) The volcano plot shows significant differences in genes between the early (ESPL and non-mESCC) and advanced (mESCC and mLN) stages of ESCC. (B) Pathway enrichment analysis of differentially expressed genes in the early and advanced stages of ESCC. (C) The gene expression levels associated with significantly enriched pathways throughout the occurrence and development of ESCC. (D) mIF staining of CCND1, LAMB1, and IL-18 on ESCC tissues. Scale bar, 200 μm. (E) Comparison of the percentages of CCND1, LAMB1, and IL-18-positive cells on ESCC tissues. Box plots show the median and interquartile range, whiskers extend to 1.5 × IQR. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, p values were calculated using a two-sided Wilcoxon rank-sum test. (F) The heatmap of gradient-changed DEGs based on pseudotime and ESCC progression of EP.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Gene Expression, Staining, Comparison

OGT promotes ESCC progression through regulating proliferation, migration, invasion, and apoptosis in vitro and in vivo (A) Representative images of immunohistochemical staining for OGT in cancer and adjacent tissues, magnified at 200× and 400×; scale bars, 100 μm. (B) Paired comparison of OGT IHC scores in tumor and peritumor tissues. p value was calculated using a two-sided Wilcoxon signed-rank test (paired samples, n = 76). (C) Representative WB images of OGT and O-GlcNAc level in all transient transfection groups, including knockdown in KYSE30 and KYSE450 (transfected with siNC, si OGT #1, or si OGT #2) and overexpress in KYSE150 and KYSE410 (transfected with oeVector, oe OGT , or oe OGT and treated with OSMI-1). Images are representative of three independent experiments ( n = 3). (D) OGT and O-GlcNAc level in lentiviral-mediated knockdown KYSE450 and overexpress KYSE150. Representative protein images of three independent experiments were shown ( n = 3). (E and F) Representative images and quantification of plate clone formation assay of lentiviral-mediated knockdown KYSE450 and overexpress KYSE150 cell lines. Data are mean ± SD from three independent experiments ( n = 3). p values were calculated using one-way ANOVA. (G) Cell proliferation measured by the CCK8 assay and relative cell proliferation quantified by OD value at 450 nm of KYSE30, KYSE450, KYSE150, and KYSE410 cell lines. Data are presented as mean ± SD from three independent experiments ( n = 3). p values were calculated using two-way ANOVA with Tukey's multiple-comparisons test. (H) Representative images of cell migration and invasion assays in the KYSE30, KYSE450, KYSE150, and KYSE410 cell lines ( n = 3). Scale bars, 200 μm. (I) Stably transfected shNC/sh OGT KYSE450 cell subcutaneously injected into nude mice. Representative image of xenograft tumors and tumor volume from day 5 to day 30. Data are presented as mean ± SD, n = 5 mice per group. p values were calculated using two-way repeated-measures ANOVA with Sidak's multiple-comparisons test. (J) Bioluminescence imaging of lung metastatic foci at the 7th week in a lung metastasis model. Luciferase activity is measured in photons per cm2 per second per steradian (p/s/cm2/sr). (K) Representative images and quantitative analysis of metastasis nodules on the lung surface. Arrowheads denote the metastasis nodules on the lung surface. (L) Representative images of HE staining of lung metastasis and quantitative analysis of lung metastasis area. Arrowheads denote the metastasis nodules. Scale bars, 200 μm. (J–L) Data are presented as mean ± SD, n = 5 mice per group. p values were calculated using a two-sided Wilcoxon rank-sum test. (M) The results of enriched pathways affected by OGT expression detected across different omics. In the RNA-seq dataset, siOGT cells were defined as the OGT low group, while siNC cells were defined as the OGT-high group. In both the proteomic and glycoproteomic datasets, oeVector cells were defined as the OGT-low group, and oeOGT cells were defined as the OGT-high group. Pathways activated in the OGT-high group are marked in green, while pathways inhibited are marked in red. (N) Comparison of apoptosis rate between KYSE450 siNC and si OGT groups. Data are presented as mean ± SD, n = 3 per group. p values were calculated using unpaired Student's t test. (O) Flow cytometry analysis of cell cycle distribution of KYSE450 cells across siNC and si OGT . ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. NC, negative control group.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: OGT promotes ESCC progression through regulating proliferation, migration, invasion, and apoptosis in vitro and in vivo (A) Representative images of immunohistochemical staining for OGT in cancer and adjacent tissues, magnified at 200× and 400×; scale bars, 100 μm. (B) Paired comparison of OGT IHC scores in tumor and peritumor tissues. p value was calculated using a two-sided Wilcoxon signed-rank test (paired samples, n = 76). (C) Representative WB images of OGT and O-GlcNAc level in all transient transfection groups, including knockdown in KYSE30 and KYSE450 (transfected with siNC, si OGT #1, or si OGT #2) and overexpress in KYSE150 and KYSE410 (transfected with oeVector, oe OGT , or oe OGT and treated with OSMI-1). Images are representative of three independent experiments ( n = 3). (D) OGT and O-GlcNAc level in lentiviral-mediated knockdown KYSE450 and overexpress KYSE150. Representative protein images of three independent experiments were shown ( n = 3). (E and F) Representative images and quantification of plate clone formation assay of lentiviral-mediated knockdown KYSE450 and overexpress KYSE150 cell lines. Data are mean ± SD from three independent experiments ( n = 3). p values were calculated using one-way ANOVA. (G) Cell proliferation measured by the CCK8 assay and relative cell proliferation quantified by OD value at 450 nm of KYSE30, KYSE450, KYSE150, and KYSE410 cell lines. Data are presented as mean ± SD from three independent experiments ( n = 3). p values were calculated using two-way ANOVA with Tukey's multiple-comparisons test. (H) Representative images of cell migration and invasion assays in the KYSE30, KYSE450, KYSE150, and KYSE410 cell lines ( n = 3). Scale bars, 200 μm. (I) Stably transfected shNC/sh OGT KYSE450 cell subcutaneously injected into nude mice. Representative image of xenograft tumors and tumor volume from day 5 to day 30. Data are presented as mean ± SD, n = 5 mice per group. p values were calculated using two-way repeated-measures ANOVA with Sidak's multiple-comparisons test. (J) Bioluminescence imaging of lung metastatic foci at the 7th week in a lung metastasis model. Luciferase activity is measured in photons per cm2 per second per steradian (p/s/cm2/sr). (K) Representative images and quantitative analysis of metastasis nodules on the lung surface. Arrowheads denote the metastasis nodules on the lung surface. (L) Representative images of HE staining of lung metastasis and quantitative analysis of lung metastasis area. Arrowheads denote the metastasis nodules. Scale bars, 200 μm. (J–L) Data are presented as mean ± SD, n = 5 mice per group. p values were calculated using a two-sided Wilcoxon rank-sum test. (M) The results of enriched pathways affected by OGT expression detected across different omics. In the RNA-seq dataset, siOGT cells were defined as the OGT low group, while siNC cells were defined as the OGT-high group. In both the proteomic and glycoproteomic datasets, oeVector cells were defined as the OGT-low group, and oeOGT cells were defined as the OGT-high group. Pathways activated in the OGT-high group are marked in green, while pathways inhibited are marked in red. (N) Comparison of apoptosis rate between KYSE450 siNC and si OGT groups. Data are presented as mean ± SD, n = 3 per group. p values were calculated using unpaired Student's t test. (O) Flow cytometry analysis of cell cycle distribution of KYSE450 cells across siNC and si OGT . ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. NC, negative control group.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Migration, In Vitro, In Vivo, Immunohistochemical staining, Staining, Comparison, Transfection, Knockdown, Tube Formation Assay, CCK-8 Assay, Stable Transfection, Injection, Imaging, Luciferase, Activity Assay, Expressing, RNA Sequencing, Flow Cytometry, Negative Control

Changes in TME during the progression of ESCC (A) Abundance of 17 cells estimated by SpatialDecon algorithm in non-EP compartments between the early (ESPL and non-mESCC) and advanced stages (mESCC and mLN) of ESCC. (B) Comparison of proportion of presented cells between the early and advanced stages of ESCC. Box plot shows the median and interquartile range, whiskers extend to 1.5 × IQR. p values were calculated using two-sided Wilcoxon rank-sum test. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (C) Volcano plot showing the DEGs between early and advanced stages in ST compartment. (D) Volcano plot showing the DEGs between early and advanced stages in MC compartment. (E) Volcano plot showing the DEGs between early and advanced stages in NC compartment. (F) Cell-cell interactions based on significant ligand-receptor pairs in advanced stages of ESCC. (G) Interaction relationships of the ACTIVIN, CHEMERIN, and PERIOSTIN pathways among compartments in advanced ESCC. (H) Cell-cell interactions between ST compartments and other compartments via the ACTIVIN, CHEMERIN, and PERIOSTIN pathways during ESCC initiation and progression. (I) The four-quadrant diagram showed the significant differences in gene expression patterns among three different types in the TLS during the ESCC process. Genes showing continuous increase were marked in red, while genes showing continuous decrease were marked in blue. (J) Volcano plot showed significant differentially expressed genes between the TLS of tumor and the lymph follicles of lymph nodules.

Journal: Cell Reports Medicine

Article Title: Spatial omics study reveals molecular-cellular dynamics of tumor ecosystem in esophageal squamous-cell carcinoma initiation and progression

doi: 10.1016/j.xcrm.2026.102650

Figure Lengend Snippet: Changes in TME during the progression of ESCC (A) Abundance of 17 cells estimated by SpatialDecon algorithm in non-EP compartments between the early (ESPL and non-mESCC) and advanced stages (mESCC and mLN) of ESCC. (B) Comparison of proportion of presented cells between the early and advanced stages of ESCC. Box plot shows the median and interquartile range, whiskers extend to 1.5 × IQR. p values were calculated using two-sided Wilcoxon rank-sum test. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (C) Volcano plot showing the DEGs between early and advanced stages in ST compartment. (D) Volcano plot showing the DEGs between early and advanced stages in MC compartment. (E) Volcano plot showing the DEGs between early and advanced stages in NC compartment. (F) Cell-cell interactions based on significant ligand-receptor pairs in advanced stages of ESCC. (G) Interaction relationships of the ACTIVIN, CHEMERIN, and PERIOSTIN pathways among compartments in advanced ESCC. (H) Cell-cell interactions between ST compartments and other compartments via the ACTIVIN, CHEMERIN, and PERIOSTIN pathways during ESCC initiation and progression. (I) The four-quadrant diagram showed the significant differences in gene expression patterns among three different types in the TLS during the ESCC process. Genes showing continuous increase were marked in red, while genes showing continuous decrease were marked in blue. (J) Volcano plot showed significant differentially expressed genes between the TLS of tumor and the lymph follicles of lymph nodules.

Article Snippet: KYSE30 human ESCC cell line , Servicebio , STCC11903P.

Techniques: Comparison, Gene Expression