European journal of medical research · 2025
TIGD6 in gastric cancer: exploring its prognostic value and therapeutic potential through molecular and clinical investigations.
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Han Quanli, Deng Muhong, Cui Zhi, Wang Qi, Li Dongbing
Аннотация
BACKGROUND: Gastric cancer (GC) predominantly contributes to cancer mortality, with adenocarcinomas accounting for more than 95% of incidences. Early detection improves survival, but most cases are diagnosed at advanced stages due to subtle symptoms and rapid progression. The role of TIGD6 in GC is unclear.
METHODS: We analyzed TIGD6 expression using TCGA data and correlated it with clinical features and outcomes in GC patients. Bioinformatics tools, including GSEA and single-cell sequencing, were used to elucidate TIGD6's role in GC. In the GC cell lines AGS and HGC-27, TIGD6 was knocked down using RNA interference, and subsequent in vitro experiments were conducted to evaluate cell proliferation, migration, and invasion capabilities.
RESULTS: The expression of TIGD6 was markedly elevated in GC tissues relative to normal tissues (p < 0.001). Higher TIGD6 levels were linked to residual tumors (p = 0.027), history of reflux (p = 0.019), and antireflux treatment (p = 0.0012). Increased TIGD6 expression was associated with decreased overall survival (OS, p = 0.009) and disease-specific survival (DSS, p = 0.008), and it served as an independent predictor of worse OS (p = 0.043). Knocking down TIGD6 in GC cells suppressed proliferation, migration, and invasion, while enhancing apoptosis through modulation of the Hedgehog signaling pathway.
CONCLUSION: TIGD6 is overexpressed in GC and linked to unfavorable outcomes. It could potentially function as a biomarker and therapeutic target for this malignancy. Future studies should validate its clinical relevance and explore its detailed molecular mechanisms. Collectively, this study provides the first functional, mechanistic, and immune-phenotypic characterization of TIGD6 in GC, positioning it as a dual biomarker and therapeutic target.
METHODS: We analyzed TIGD6 expression using TCGA data and correlated it with clinical features and outcomes in GC patients. Bioinformatics tools, including GSEA and single-cell sequencing, were used to elucidate TIGD6's role in GC. In the GC cell lines AGS and HGC-27, TIGD6 was knocked down using RNA interference, and subsequent in vitro experiments were conducted to evaluate cell proliferation, migration, and invasion capabilities.
RESULTS: The expression of TIGD6 was markedly elevated in GC tissues relative to normal tissues (p < 0.001). Higher TIGD6 levels were linked to residual tumors (p = 0.027), history of reflux (p = 0.019), and antireflux treatment (p = 0.0012). Increased TIGD6 expression was associated with decreased overall survival (OS, p = 0.009) and disease-specific survival (DSS, p = 0.008), and it served as an independent predictor of worse OS (p = 0.043). Knocking down TIGD6 in GC cells suppressed proliferation, migration, and invasion, while enhancing apoptosis through modulation of the Hedgehog signaling pathway.
CONCLUSION: TIGD6 is overexpressed in GC and linked to unfavorable outcomes. It could potentially function as a biomarker and therapeutic target for this malignancy. Future studies should validate its clinical relevance and explore its detailed molecular mechanisms. Collectively, this study provides the first functional, mechanistic, and immune-phenotypic characterization of TIGD6 in GC, positioning it as a dual biomarker and therapeutic target.