Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: Top 20 upregulated protein molecules modulated by CDDO-Me in Ec109 cells

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques:

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: The top ten canonical signaling pathways regulated by CDDO-Me in Ec109 cells analyzed by ingenuity pathway analysis. Abbreviations: CDDO-Me, methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; eIF2, eukaryotic initiation factor 2; p70S6K, p70S6 kinase; mTOR, mammalian target of rapamycin; RAN, ras-related nuclear protein; Nrf2, nuclear factor (erythroid-derived 2)-like 2.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques: Protein-Protein interactions, Derivative Assay

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: Representative blots of protein levels of VKORC1, CaMKIIα, NPLOC4, PSME3, and Dynamin 2 in various human ESCC cell lines and normal human esophageal epithelial cell line (Het-1A) were determined using Western blot analysis. β-Actin served as loading controls. Abbreviations: VKORC1, vitamin K epoxide reductase complex subunit 1; CaMKIIα, calcium/calmodulin-dependent protein kinase type II subunit alapha; NPLOC4, nuclear protein localization protein 4 homolog; PSME3, proteasome activator complex subunit 3; ESCC, esophageal squamous cell carcinoma.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques: Western Blot

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: Mitochondrial dysfunction signaling pathway regulated by CDDO-Me in Ec109 cells. Notes: Ec109 cells were treated with 0.5 μM CDDO-Me for 24 hours and the protein samples were subject to quantitative proteomic analysis. Red indicates an upregulation; green indicates a downregulation. The intensity of green and red molecule colors indicates the degree of down- or upregulation, respectively. Solid arrows indicate direct interaction and dashed arrows indicate indirect interaction. Abbreviations: CDDO-Me, methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques:

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: mTOR signaling pathway regulated by CDDO-Me in Ec109 cells. Notes: Ec109 cells were treated with 0.5 μM CDDO-Me for 24 hours and the protein samples were subject to quantitative proteomic analysis. Red indicates an upregulation; green indicates a downregulation. The intensity of green and red molecule colors indicates the degree of down- or upregulation, respectively. Solid arrows indicate direct interaction and dashed arrows indicate indirect interaction. Abbreviation: CDDO-Me, methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; mTOR, mammalian target of rapamycin.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques:

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: The effect of knockdown of CaMKIIα on the CDDO-Me induced apoptosis in human ESCC cells. A. Percentages of specific cell populations showed in dot plots and apoptotic cells showed in bar graphs for the silencing of CaMKIIα in Ec109 and KYSE30 cells with or without 0.5 μM CDDO-Me treatment for 24 hours. B. Representative blots of bcl-2, bax, and cleaved caspase-3 for the proteinlysate samples, which were prepared from Ec109 and KYSE30 cells treated with CaMKIIα siRNAs or 0.5 μM CDDO-Me for 24 hours. Abbreviation: CaMKIIα, calcium/calmodulin-dependent protein kinase type II subunit alapha; CDDO-Me, methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; ESCC, esophageal squamous cell carcinoma; bcl-2, B-cell lymphoma-2; bax, bcl-2 associated X protein; siRNA , small interfering RNA.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques: Knockdown, Small Interfering RNA

Journal: American Journal of Translational Research

Article Title: The therapeutic response of CDDO-Me in the esophageal squamous cell carcinoma (ESCC) cells is mediated by CaMKIIα

doi:

Figure Lengend Snippet: The effect of knockdown of CaMKIIα on the CDDO-Me induced autophagy in human ESCC cells. A. Percentages of specific cell populations showed in dot plots and autophagic cells showed in bar graphs for the silencing of CaMKIIα in Ec109 and KYSE30 cells with or without 0.5 μM CDDO-Me treatment for 24 hours. B. CDDO-Me-induced autophagic death in the silencing of CaMKIIα in Ec109 and KYSE30 cellsdetermined by confocal microscopy. The level of autophagy was evaluated using a lysosome-specific fluorescence dye. The confocal microscopic images of autophagic Ec109 and KYSE 30 cells (stained in green) are also shown. C. Representative blots of beclin-1 and LC3I/II for the proteinlysate samples, which were prepared from Ec109 and KYSE30 cells treated with CaMKIIα siRNAs or 0.5 μM CDDO-Me for 24 hours. Abbreviation: CaMKIIα, calcium/calmodulin-dependent protein kinase type II subunit alapha; CDDO-Me, methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; ESCC, esophageal squamous cell carcinoma; siRNA, small interfering RNA; LC 3, microtubule-associated protein 1A/1B-light chain 3.

Article Snippet: Human ESCC Ec109 cells was obtained from AddexBio Inc. (San Diego, CA, USA), KYSE70 and KYSE30 cells were obtained from Sigma-Aldrich Co (St Louis, MO, USA).

Techniques: Knockdown, Confocal Microscopy, Fluorescence, Staining, Small Interfering RNA

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Construction of a risk signature using the least absolute shrinkage and selection operator (LASSO) analysis. Partial likelihood deviances for (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Coefficient profiles of senescence‐related gene pairs for (C) ESCC and (D) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Selection

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Kaplan–Meier analysis of high‐ and low‐risk patients (red and blue, respectively) with (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Receiver operating characteristic curves for (C) ESCC and (D) EAC. Survival risk curves (top) and sand scatter plots (bottom) for (E) ESCC and (F) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Correlations of immune microenvironments evaluated using ESTIMATE. (A) Immune score and (B) ESTIMATE score for oesophageal squamous cell carcinoma (ESCC). (C) Immune score and (D) ESTIMATE score for oesophageal adenocarcinoma (EAC). Relationships between risk and immune scores for (E) ESCC and (H) EAC. Relationships between risk and ESTIMATE scores for (F) ESCC and (G) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Random forest error rates (left graphs) and relative importance (right graphs) for (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Expression of IRF5 and BMI1 in (C) ESCC, (D) EAC and (E) EC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Expression analyses of IRF5 in four ESCC cell lines using western blotting (A, B). The efficiency of IRF5 ‐knockdown in KYSE150 cells was determined using western blotting (C, D). Ctrl: No siRNA infection; NC: Negative control. Statistical analyses of n = 3 independent experiments were assessed. Results are shown as mean ± SD, ns p ≥ 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Expressing, Western Blot, Knockdown, Infection, Negative Control

Journal: Nature Communications

Article Title: Nuclear ANLN regulates transcription initiation related Pol II clustering and target gene expression

doi: 10.1038/s41467-025-56645-9

Figure Lengend Snippet: A KYSE150 cells were treated with 0.1 μM THZ1 for 3 h, ANLN (pink) and Pol II (green) clusters were observed with super-resolution imaging. Scale bar, 3 μm. B , C Effect of THZ1 on the number of different types of clusters. n = 42 (Control); n = 45 (THZ1). The error bars indicate the mean ± SDs. Two-tailed Student’s t tests were performed to determine the significance. D Relative fluorescence intensity of protein signals per cell per focal plane. n = 42 (Control); n = 45 (THZ1). The error bars indicate the mean ± SDs. Two-tailed Student’s t tests were performed to determine the significance. E , F Heatmap ( E ) and box plots ( F ) showing expression changes of all protein-coding genes (Total, n = 11376), super-enhancer-associated genes (SE, n = 652), and target genes (TG, n = 84) with or without THZ1 treatment. The error bars indicate the mean ± SDs. Two-tailed Student’s t tests were performed to determine the significance. G KYSE150 cells were treated with 0.1 μM THZ1, the mRNA expression of the indicated target genes was measured. The error bars indicate the mean ± SDs. Two-tailed Student’s t tests were performed to determine the significance. H The indicated cell lines were treated with different concentrations of THZ1 for 48 h, and cell viability was subsequently analyzed by MTS assay. The error bars indicate the mean ± SDs. I ESCC cell lines were treated with low toxicity THZ1 (0.04 μM) or/and F806 (20 μM) for 48 h, and cell viability was measured by MTS assay. n = 3 for each group. The error bars indicate the mean ± SDs. The data are representative of at least three independent experiments with similar results. Source data are provided as a Source Data file.

Article Snippet: ESCC cell lines were established and provided by Dr. Shimada Yutaka (Faculty of Medicine, Kyoto University, Japan) and Dr. Nishihira (Tohoku University School of Medicine, Japan) – .

Techniques: Imaging, Control, Two Tailed Test, Fluorescence, Expressing, MTS Assay

Journal: Cancer Medicine

Article Title: Aberrant DNA hypermethylation reduces the expression of the desmosome-related molecule periplakin in esophageal squamous cell carcinoma

doi: 10.1002/cam4.369

Figure Lengend Snippet: PPL expression was silenced by DNA methylation in ESCC. (A) Typical images of formalin-fixed, paraffin-embedded samples of ESCC, and adjacent noncancerous mucosa (normal) stained with H&E or anti-PPL antibody. (B) PPL transcript levels in paired samples from 13 ESCC samples were determined by RT-PCR. Data indicate expression relative to the mean levels of normal tissues. (C) DNA methylation of PPL as determined by pyrosequencing of paired samples from 17 patients with ESCC. (D) Expression of PPL in ESCC relative to that in normal tissue plotted against the change in DNA methylation (ratio of tumor to normal tissue) in each paired sample. (E) PPL mRNA induction in ESCC cell lines after treatment with 1 or 5 μ mol/L of 5-aza-dC. The fold increase in induction in the treated cells relative to that in the untreated cells is shown for each cell line. Data are shown as mean + SD of duplicated assays. *Difference from untreated cells was statistically significant ( P < 0.05). (F) KYSE270 cells were treated with the indicated concentrations of 5-aza-dC. The levels of methylation of PPL DNA (left Y axis, solid lines) and mRNA (right Y axis, dotted lines) are shown. Data are shown as mean ± SD of triplicated assays. *Difference from untreated cells was statistically significant ( P < 0.05). (G) KYSE270 cells were treated with 5 μ mol/L of 5-aza-dC, and stained with anti-PPL antibody (green) and DAPI for nuclear staining (red). ESCC, esophageal squamous cell carcinoma; PPL, periplakin.

Article Snippet: Human ESCC lines KYSE70, KYSE140, KYSE150, KYSE270, KYSE410, and KYSE510 were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan) on 13 August 2013.

Techniques: Expressing, DNA Methylation Assay, Formalin-fixed Paraffin-Embedded, Staining, Reverse Transcription Polymerase Chain Reaction, Methylation

Journal: Cancer Medicine

Article Title: Aberrant DNA hypermethylation reduces the expression of the desmosome-related molecule periplakin in esophageal squamous cell carcinoma

doi: 10.1002/cam4.369

Figure Lengend Snippet: Forced PPL expression induced desmosome-like structures. (A) TEM images were obtained from normal human esophageal mucosa (normal) and mock-transfected or PPL-transfected KTSE270 cells at 10,000× or 30,000× magnification. Desmosomes were frequently found in normal tissues and PPL-transfected cells (arrows). In the images of the mock-transfected cells taken at 10,000× magnification, the arrow indicates adhesion plaque-like structures, which was not identified as a desmosome at higher magnification. (B) Expression of envoplakin (EVPL) in mock- or PPL- transfected KYSE270 cells. EVPL mRNA levels were shown as fold expression of the levels to normal esophageal mucosa (average of 13 mucosa = 1). Data are shown as mean + SD of three assays. (C) Expression of envoplakin (EVPL) in ESCC tissues with paired normal mucosa. PPL, periplakin; ESCC, esophageal squamous cell carcinoma.

Article Snippet: Human ESCC lines KYSE70, KYSE140, KYSE150, KYSE270, KYSE410, and KYSE510 were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan) on 13 August 2013.

Techniques: Expressing, Transfection