Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
ANKRD1 expression and functional mechanism in stomach adenocarcinoma.
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Nie Lu, Nie Yu, Wang Ruiyang
Аннотация
BACKGROUND: ANKRD1 is implicated in various cancers, but its role in stomach adenocarcinoma (STAD) remains unclear.
METHODS: ANKRD1 expression and its prognostic value in STAD were analyzed using TIMER, UALCAN, GEPIA, and Kaplan-Meier plotter. Immune cell infiltration was evaluated via CIBERSORT and Single-sample Gene Set Enrichment Analysis (ssGSEA). Somatic mutations were analyzed from TCGA data. Functional enrichment analysis (GO, KEGG, GSEA (Gene Set Enrichment Analysis)) was performed on ANKRD1-associated genes. Subsequently, in vitro experiments were conducted. ANKRD1 protein levels were examined in STAD cell lines by Western blot. Stable knockdown and overexpression models were created. Functional assays (CCK-8, Transwell, and wound healing) assessed proliferation, migration, and invasion. Western blot measured STAT3 pathway activity.
RESULTS: ANKRD1 was significantly overexpressed in STAD tissues, and high expression correlated with poorer overall, first progression, and post-progression survival. ANKRD1 expression positively correlated with M0 macrophage and activated mast cell infiltration and negatively with resting memory CD4 + T cells and naive B cells. Although ANKRD1 itself was not mutated, associated genes were enriched in pathways like Wnt signaling. In vitro, ANKRD1 knockdown inhibited cell proliferation, migration, and invasion, while its overexpression promoted these effects. ANKRD1 was found to modulate STAT3 phosphorylation.
CONCLUSIONS: ANKRD1 is overexpressed in STAD and predicts poor prognosis. It promotes tumor cell proliferation, migration, and invasion, likely through activating the STAT3 signaling pathway, and correlates with an altered immune microenvironment.
METHODS: ANKRD1 expression and its prognostic value in STAD were analyzed using TIMER, UALCAN, GEPIA, and Kaplan-Meier plotter. Immune cell infiltration was evaluated via CIBERSORT and Single-sample Gene Set Enrichment Analysis (ssGSEA). Somatic mutations were analyzed from TCGA data. Functional enrichment analysis (GO, KEGG, GSEA (Gene Set Enrichment Analysis)) was performed on ANKRD1-associated genes. Subsequently, in vitro experiments were conducted. ANKRD1 protein levels were examined in STAD cell lines by Western blot. Stable knockdown and overexpression models were created. Functional assays (CCK-8, Transwell, and wound healing) assessed proliferation, migration, and invasion. Western blot measured STAT3 pathway activity.
RESULTS: ANKRD1 was significantly overexpressed in STAD tissues, and high expression correlated with poorer overall, first progression, and post-progression survival. ANKRD1 expression positively correlated with M0 macrophage and activated mast cell infiltration and negatively with resting memory CD4 + T cells and naive B cells. Although ANKRD1 itself was not mutated, associated genes were enriched in pathways like Wnt signaling. In vitro, ANKRD1 knockdown inhibited cell proliferation, migration, and invasion, while its overexpression promoted these effects. ANKRD1 was found to modulate STAT3 phosphorylation.
CONCLUSIONS: ANKRD1 is overexpressed in STAD and predicts poor prognosis. It promotes tumor cell proliferation, migration, and invasion, likely through activating the STAT3 signaling pathway, and correlates with an altered immune microenvironment.