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Keygen Biotech gastric epithelial cell line ges 1
Gastric Epithelial Cell Line Ges 1, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ges-1+cell+line/ags+cancer+cell+ddp+gastric+line+resistant/pm41317224-45-4-21
Average 86 stars, based on 1 article reviews
gastric epithelial cell line ges 1 - by Bioz Stars, 2026-09
86/100 stars

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Cell Culture:

Article Title: Stimulating TRPM7 Suppresses Cancer Cell Proliferation and Metastasis by Inhibiting Autophagy
Article Snippet: Co., Ltd. MCF-7, MCF-10A, A-375, U-87 MG, SGC7901, and GES-1 were obtained from KeyGEN BioTECH.

Article Title: Long non-coding RNA MIAT promotes gastric cancer proliferation and metastasis via modulating the miR-331-3p/RAB5B pathway
Article Snippet: The human gastric epithelial mucosa cell line GES-1 and GC cell lines HGC-27, AGS, MKN45 and NCI-N87 were purchased from Nanjing Keygen Biotech Co., Ltd. HGC-27, AGS, MKN45 and NCI-N87 cells were maintained in RPMI-1640 with 10% foetal bovine serum (FBS), 100 U/ml penicillin and 100 μg/ml streptomycin (HyClone; GE Healthcare Life Sciences).

Article Title: Ghrelin inhibition of ethanol-induced gastric epithelial cell apoptosis is mediated by miR-21
Article Snippet: Cell culture The human gastric epithelial cell line, GES-1 (KeyGen Biotech, Nanjing, Jiangsu, China), was maintained in 90% DMEM (Invitrogen, Carlsbad, CA, USA) and 10% fetal bovine serum (FBS; ExCell Biology, Shanghai, China) supplemented with penicillin and streptomycin (Invitrogen) at 37°C in a humidified atmosphere containing 5% CO 2 .

Article Title: COL5A1 Promotes the Progression of Gastric Cancer by Acting as a ceRNA of miR-137-3p to Upregulate FSTL1 Expression
Article Snippet: The human gastric epithelial cell line GES-1 and GC cell lines AGS, HGC27, MGC803, and MKN45 were purchased from KeyGEN BioTECH (Nanjing, China).

Article Title: Stimulating TRPM7 suppresses cancer cell proliferation and metastasis by inhibiting autophagy.
Article Snippet: Co., Ltd. MCF-7, MCF-10A, A-375, U-87 MG, SGC-7901, and GES-1 were obtained from KeyGEN BioTECH.

Article Title: Ghrelin inhibition of ethanol-induced gastric epithelial cell apoptosis is mediated by miR-21
Article Snippet: The human gastric epithelial cell line, GES-1 (KeyGen Biotech, Nanjing, Jiangsu, China), was maintained in 90% DMEM (Invitrogen, Carlsbad, CA, USA) and 10% fetal bovine serum (FBS; ExCell Biology, Shanghai, China) supplemented with penicillin and streptomycin (Invitrogen) at 37°C in a humidified atmosphere containing 5% CO 2 .



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A, B Kaplan-Meier analysis of 5-year Disease-free survival (DFS) and overall survival (OS) of 242 STAD patients in our center stratified by ODC1 expression. While curves showing high ODC1 group had shorter progression-free intervals. C HPA database reference confirming ODC1 protein overexpression in STAD tissues. D , E Immunohistochemical (IHC) analysis performed on a tissue microarray constructed from surgical specimens at our center confirmed that ODC1 is highly expressed in gastric cancer tissues by Semi-quantitative H-score analysis. F RT-qPCR of ODC1 mRNA in 18 paired clinical specimens. G Western blot quantification showing ODC1 increase in tumors. H RT-qPCR analysis across gastric cell lines confirming cancer cell-specific ODC1 elevation (vs. <t>GES-1).</t> I ODC1 protein expression levels in seven STAD cell lines and non-tumor cell line GES-1. Data are marked as the means ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.
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A, B Kaplan-Meier analysis of 5-year Disease-free survival (DFS) and overall survival (OS) of 242 STAD patients in our center stratified by ODC1 expression. While curves showing high ODC1 group had shorter progression-free intervals. C HPA database reference confirming ODC1 protein overexpression in STAD tissues. D , E Immunohistochemical (IHC) analysis performed on a tissue microarray constructed from surgical specimens at our center confirmed that ODC1 is highly expressed in gastric cancer tissues by Semi-quantitative H-score analysis. F RT-qPCR of ODC1 mRNA in 18 paired clinical specimens. G Western blot quantification showing ODC1 increase in tumors. H RT-qPCR analysis across gastric cell lines confirming cancer cell-specific ODC1 elevation (vs. <t>GES-1).</t> I ODC1 protein expression levels in seven STAD cell lines and non-tumor cell line GES-1. Data are marked as the means ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.
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Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line <t>(GES-1)</t> and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA
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Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line <t>(GES-1)</t> and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA
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Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line <t>(GES-1)</t> and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA
Gastric Epithelial Cell Line Ges 1, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ges-1+cell+line/ags+cancer+cell+ddp+gastric+line+resistant/pm41317224-45-4-21
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Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line <t>(GES-1)</t> and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA
Normal Human Gastric Epithelial Cell Line Ges 1, 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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A, B Kaplan-Meier analysis of 5-year Disease-free survival (DFS) and overall survival (OS) of 242 STAD patients in our center stratified by ODC1 expression. While curves showing high ODC1 group had shorter progression-free intervals. C HPA database reference confirming ODC1 protein overexpression in STAD tissues. D , E Immunohistochemical (IHC) analysis performed on a tissue microarray constructed from surgical specimens at our center confirmed that ODC1 is highly expressed in gastric cancer tissues by Semi-quantitative H-score analysis. F RT-qPCR of ODC1 mRNA in 18 paired clinical specimens. G Western blot quantification showing ODC1 increase in tumors. H RT-qPCR analysis across gastric cell lines confirming cancer cell-specific ODC1 elevation (vs. GES-1). I ODC1 protein expression levels in seven STAD cell lines and non-tumor cell line GES-1. Data are marked as the means ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.

Journal: Cell Death Discovery

Article Title: Targeting the ODC1-YBX1 axis reverses gastric cancer chemoresistance via transcriptional control of SLC7A11-mediated ferroptosis

doi: 10.1038/s41420-026-03067-1

Figure Lengend Snippet: A, B Kaplan-Meier analysis of 5-year Disease-free survival (DFS) and overall survival (OS) of 242 STAD patients in our center stratified by ODC1 expression. While curves showing high ODC1 group had shorter progression-free intervals. C HPA database reference confirming ODC1 protein overexpression in STAD tissues. D , E Immunohistochemical (IHC) analysis performed on a tissue microarray constructed from surgical specimens at our center confirmed that ODC1 is highly expressed in gastric cancer tissues by Semi-quantitative H-score analysis. F RT-qPCR of ODC1 mRNA in 18 paired clinical specimens. G Western blot quantification showing ODC1 increase in tumors. H RT-qPCR analysis across gastric cell lines confirming cancer cell-specific ODC1 elevation (vs. GES-1). I ODC1 protein expression levels in seven STAD cell lines and non-tumor cell line GES-1. Data are marked as the means ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.

Article Snippet: The human gastric epithelial cell line GES-1 and gastric cancer cell lines NCI-N87, AGS, SUN-719, MKN-1, MKN-45, SUN-484, and HGC-27 were sourced from ProCell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: Expressing, Over Expression, Immunohistochemical staining, Microarray, Construct, Quantitative RT-PCR, Western Blot

Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line (GES-1) and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA

Journal: World Journal of Surgical Oncology

Article Title: Analysis of the proliferative role and prognostic value of GPR173 in gastric cancer

doi: 10.1186/s12957-026-04274-x

Figure Lengend Snippet: Impact of GPR173 on gastric cancer cell proliferation in vitro and in vivo. A Relative mRNA expression of GPR173 in 10 pairs of gastric cancer tissues (Tumor) and adjacent Non-tumor tissues (Non-tumor) was measured by RT-qPCR. B Protein expression level of GPR173 in the human Non-tumor gastric mucosal epithelial cell line (GES-1) and various gastric cancer cell lines was detected by Western blot. C Western blot analysis validating the knockdown efficiency of GPR173 in MKN-45 cells and overexpression efficiency in AGS cells at the protein level. GAPDH served as the loading control. D The relative mRNA expression of GPR173 in MKN-45 cells transfected with different siRNAs (si-1, si-2, si-3) compared to negative control (NC) was determined by RT-qPCR. E The relative mRNA expression of GPR173 in AGS cells transfected with GPR173 overexpression plasmid (OE) compared to empty vector (Vector) was confirmed by RT-qPCR. F , H A colony formation assay and its quantification showed that knockdown of GPR173 inhibited the colony-forming ability of MKN-45 cells. G , H A colony formation assay and its quantification indicated that overexpression of GPR173 (OE) enhanced the colony-forming ability of AGS cells. I , K An EdU incorporation assay and its quantification revealed that knockdown of GPR173 suppressed the proliferation of MKN-45 cells. J , K An EdU incorporation assay and its quantification demonstrated that overexpression of GPR173 promoted the proliferation of AGS cells. L A CCK-8 assay showed that GPR173 knockdown inhibited the viability of MKN-45 cells. M A CCK-8 assay indicated that GPR173 overexpression enhanced the viability of AGS cells. N Representative images of subcutaneous xenograft tumors in nude mice injected with GPR173-overexpressing AGS cells (OE-GPR173) or control cells (Vector). O Quantitative comparison of tumor weights from each group at the experimental endpoint. P Tumor growth curves showing changes in tumor volume over time for each group. Q Representative images of IHC staining for GPR173 and the proliferation marker Ki-67 in subcutaneous xenograft tumors. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using Student’s t-test for comparisons between two groups A , D - O and one-way ANOVA for multiple comparisons. Tumor growth curves P were analyzed using two-way ANOVA

Article Snippet: The human Non-tumor gastric epithelial cell line GES-1 and human GC cell lines (MKN-45, HGC-27, SNU-216, MKN-73, AGS) were obtained from Genechem (Shanghai, China) or the Chinese Academy of Sciences Cell Bank (Shanghai, China).

Techniques: In Vitro, In Vivo, Expressing, Quantitative RT-PCR, Western Blot, Knockdown, Over Expression, Control, Transfection, Negative Control, Plasmid Preparation, Colony Assay, CCK-8 Assay, Injection, Comparison, Immunohistochemistry, Marker, Standard Deviation