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human normal gastric cell line  (ATCC)


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    Structured Review

    ATCC human normal gastric cell line
    A Box plot of USP14 expression levels in the peritumoral tissues <t>(normal)</t> and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the <t>human</t> normal <t>gastric</t> <t>cell</t> <t>line</t> (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Human Normal Gastric Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 150 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "The deubiquitination enzyme USP14 promotes the tumourigenesis of gastric cancer by enhancing c-MYC nuclear translocation through deubiquitination of KPNA2"

    Article Title: The deubiquitination enzyme USP14 promotes the tumourigenesis of gastric cancer by enhancing c-MYC nuclear translocation through deubiquitination of KPNA2

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-025-08065-2

    A Box plot of USP14 expression levels in the peritumoral tissues (normal) and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the human normal gastric cell line (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: A Box plot of USP14 expression levels in the peritumoral tissues (normal) and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the human normal gastric cell line (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemical staining, Staining



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    99
    ATCC human normal gastric cell line
    A Box plot of USP14 expression levels in the peritumoral tissues <t>(normal)</t> and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the <t>human</t> normal <t>gastric</t> <t>cell</t> <t>line</t> (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Human Normal Gastric Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    CLS Cell Lines Service GmbH human gastric epithelial cell line ges 1
    A Box plot of USP14 expression levels in the peritumoral tissues <t>(normal)</t> and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the <t>human</t> normal <t>gastric</t> <t>cell</t> <t>line</t> (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.
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    Genechem human non tumor gastric epithelial cell line ges 1
    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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    Genechem human gastric mucosal epithelial cell line 1
    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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    Korean Cell Line Bank human gastric epithelial cell line ags cells
    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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    Servicebio Inc human gastric mucosa epithelial cell line 1
    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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    Procell Inc normal human gastric epithelial cell lines
    Identification and validation of hub genes in H. pylori-associated stomach adenocarcinoma (STAD). A Differentially expressed genes (DEGs) identified from GSE13911 and GSE54129 datasets. B Venn diagram showing 234 overlapping DEGs shared between the two datasets. C Protein–protein interaction (PPI) network constructed from common DEGs using the STRING database. D Top hub genes ranked by degree centrality using the CytoHubba plugin in Cytoscape. E RT-qPCR validation of hub gene expression in eight gastric cancer cell lines versus five normal gastric <t>epithelial</t> cell lines. F Receiver operating characteristic (ROC) curve analysis showing diagnostic performance (AUC values) of THBS2, CTNNB1, COL4A1, and E2F3 in distinguishing cancerous from normal tissues. P-value < 0.05
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    Procell Inc normal human gastric epithelial cell line ges 1
    Identification and validation of hub genes in H. pylori-associated stomach adenocarcinoma (STAD). A Differentially expressed genes (DEGs) identified from GSE13911 and GSE54129 datasets. B Venn diagram showing 234 overlapping DEGs shared between the two datasets. C Protein–protein interaction (PPI) network constructed from common DEGs using the STRING database. D Top hub genes ranked by degree centrality using the CytoHubba plugin in Cytoscape. E RT-qPCR validation of hub gene expression in eight gastric cancer cell lines versus five normal gastric <t>epithelial</t> cell lines. F Receiver operating characteristic (ROC) curve analysis showing diagnostic performance (AUC values) of THBS2, CTNNB1, COL4A1, and E2F3 in distinguishing cancerous from normal tissues. P-value < 0.05
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    Image Search Results


    A Box plot of USP14 expression levels in the peritumoral tissues (normal) and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the human normal gastric cell line (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Cell Death & Disease

    Article Title: The deubiquitination enzyme USP14 promotes the tumourigenesis of gastric cancer by enhancing c-MYC nuclear translocation through deubiquitination of KPNA2

    doi: 10.1038/s41419-025-08065-2

    Figure Lengend Snippet: A Box plot of USP14 expression levels in the peritumoral tissues (normal) and GC tumors with log-rank test P values < 0.05. B , C Kaplan–Meier analysis of progression-free survival using data from the R2 database and Kaplan-Meier Plotter database. D , E qRT-PCR and Western blot assays were used to detect the expression of USP14 in the human normal gastric cell line (GES-1) and GC cell lines (MKN-45, MGC-803, BGC-823, SGC-7901, HGC-27). F Immunohistochemical staining analysis showed the expression of USP14 in different stages of gastric cancer tissues. Scale bar(black) = 200 μm. Scale bar(red) = 50 μm. All data are expressed as the mean ± SD. Student’s t test was performed to analyze significance. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: All human GC cell lines (BGC-823, HGC-27, MGC-803, MKN-45, and SGC-7901), Human normal gastric cell line (GES-1), and human embryonic renal cell line HEK293FT were obtained from the American Type Culture Collection (ATCC, Beijing, China).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemical staining, Staining

    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

    Identification and validation of hub genes in H. pylori-associated stomach adenocarcinoma (STAD). A Differentially expressed genes (DEGs) identified from GSE13911 and GSE54129 datasets. B Venn diagram showing 234 overlapping DEGs shared between the two datasets. C Protein–protein interaction (PPI) network constructed from common DEGs using the STRING database. D Top hub genes ranked by degree centrality using the CytoHubba plugin in Cytoscape. E RT-qPCR validation of hub gene expression in eight gastric cancer cell lines versus five normal gastric epithelial cell lines. F Receiver operating characteristic (ROC) curve analysis showing diagnostic performance (AUC values) of THBS2, CTNNB1, COL4A1, and E2F3 in distinguishing cancerous from normal tissues. P-value < 0.05

    Journal: Hereditas

    Article Title: Integrative analysis of Helicobacter pylori-driven stomach adenocarcinoma reveals epigenetic deregulation, immune evasion, and therapeutic resistance

    doi: 10.1186/s41065-025-00616-z

    Figure Lengend Snippet: Identification and validation of hub genes in H. pylori-associated stomach adenocarcinoma (STAD). A Differentially expressed genes (DEGs) identified from GSE13911 and GSE54129 datasets. B Venn diagram showing 234 overlapping DEGs shared between the two datasets. C Protein–protein interaction (PPI) network constructed from common DEGs using the STRING database. D Top hub genes ranked by degree centrality using the CytoHubba plugin in Cytoscape. E RT-qPCR validation of hub gene expression in eight gastric cancer cell lines versus five normal gastric epithelial cell lines. F Receiver operating characteristic (ROC) curve analysis showing diagnostic performance (AUC values) of THBS2, CTNNB1, COL4A1, and E2F3 in distinguishing cancerous from normal tissues. P-value < 0.05

    Article Snippet: A total of eight human STAD cell lines, including MKN45, AGS, SNU-1, SNU-5, NCI-N87, HGC-27, KATO III, and MKN28 and five normal human gastric epithelial cell lines, including GES-1, HFE-145, GES-1 C, GES-1 A, and Hs738.St/Int were purchased from commercial cell repositories including ATCC (American Type Culture Collection, USA) and Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Biomarker Discovery, Construct, Quantitative RT-PCR, Gene Expression, Diagnostic Assay

    Epigenetic regulation and pathway activity of hub genes in STAD. A Promoter methylation levels of THBS2, CTNNB1, COL4A1, and E2F3 in tumor vs. normal tissues using UALCAN database. B Correlation analysis between promoter methylation and gene expression using GSCA database. C Pathway activity profiles showing functional enrichment: THBS2, COL4A1, and E2F3 activate epithelial–mesenchymal transition (EMT) pathways; CTNNB1 is associated with suppression of hormone receptor pathways; E2F3 additionally activates cell cycle-related signalling. P-value < 0.05

    Journal: Hereditas

    Article Title: Integrative analysis of Helicobacter pylori-driven stomach adenocarcinoma reveals epigenetic deregulation, immune evasion, and therapeutic resistance

    doi: 10.1186/s41065-025-00616-z

    Figure Lengend Snippet: Epigenetic regulation and pathway activity of hub genes in STAD. A Promoter methylation levels of THBS2, CTNNB1, COL4A1, and E2F3 in tumor vs. normal tissues using UALCAN database. B Correlation analysis between promoter methylation and gene expression using GSCA database. C Pathway activity profiles showing functional enrichment: THBS2, COL4A1, and E2F3 activate epithelial–mesenchymal transition (EMT) pathways; CTNNB1 is associated with suppression of hormone receptor pathways; E2F3 additionally activates cell cycle-related signalling. P-value < 0.05

    Article Snippet: A total of eight human STAD cell lines, including MKN45, AGS, SNU-1, SNU-5, NCI-N87, HGC-27, KATO III, and MKN28 and five normal human gastric epithelial cell lines, including GES-1, HFE-145, GES-1 C, GES-1 A, and Hs738.St/Int were purchased from commercial cell repositories including ATCC (American Type Culture Collection, USA) and Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Activity Assay, Methylation, Gene Expression, Functional Assay

    miRNA–mRNA regulatory network and diagnostic value of miRNAs targeting hub genes in STAD. A miRNA–mRNA interaction network constructed using the miRNet database. B Expression analysis of key miRNAs (hsa-miR-15b and hsa-miR-9-2) in STAD vs. normal tissues using UALCAN database. C Kaplan–Meier survival analysis showing no significant association between the expression of hsa-miR-9-3p and hsa-miR-9-5p and overall survival in STAD patients. D RT-qPCR validation of hsa-miR-9-3p and hsa-miR-9-5p expression in eight GC cell lines and five normal gastric epithelial cell lines, confirming their upregulation in cancer. E ROC analysis demonstrating the diagnostic accuracy of hsa-miR-9-3p (AUC = 0.81) and hsa-miR-9-5p (AUC = 0.82) for distinguishing STAD cells from normal counterparts. P-value < 0.05

    Journal: Hereditas

    Article Title: Integrative analysis of Helicobacter pylori-driven stomach adenocarcinoma reveals epigenetic deregulation, immune evasion, and therapeutic resistance

    doi: 10.1186/s41065-025-00616-z

    Figure Lengend Snippet: miRNA–mRNA regulatory network and diagnostic value of miRNAs targeting hub genes in STAD. A miRNA–mRNA interaction network constructed using the miRNet database. B Expression analysis of key miRNAs (hsa-miR-15b and hsa-miR-9-2) in STAD vs. normal tissues using UALCAN database. C Kaplan–Meier survival analysis showing no significant association between the expression of hsa-miR-9-3p and hsa-miR-9-5p and overall survival in STAD patients. D RT-qPCR validation of hsa-miR-9-3p and hsa-miR-9-5p expression in eight GC cell lines and five normal gastric epithelial cell lines, confirming their upregulation in cancer. E ROC analysis demonstrating the diagnostic accuracy of hsa-miR-9-3p (AUC = 0.81) and hsa-miR-9-5p (AUC = 0.82) for distinguishing STAD cells from normal counterparts. P-value < 0.05

    Article Snippet: A total of eight human STAD cell lines, including MKN45, AGS, SNU-1, SNU-5, NCI-N87, HGC-27, KATO III, and MKN28 and five normal human gastric epithelial cell lines, including GES-1, HFE-145, GES-1 C, GES-1 A, and Hs738.St/Int were purchased from commercial cell repositories including ATCC (American Type Culture Collection, USA) and Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Diagnostic Assay, Construct, Expressing, Quantitative RT-PCR, Biomarker Discovery