Authors
Huimin Zhang, Ran Tian, Jianheng Peng
Published in
Anti-cancer agents in medicinal chemistry. Nov 12, 2026. Epub Nov 12, 2026.
Abstract
Colon adenocarcinoma (COAD) remains a major cause of cancer morbidity and mortality. SHC-transforming protein 2 (SHC2) is an adaptor protein whose cancer-type-specific expression and biological relevance, particularly in COAD, are insufficiently defined.
This study integrated TCGA-based expression, clinicopathological, and survival analyses with cBioPortal/ GSCA genomic and methylation analyses, xCell and TIMER immune infiltration estimates, GDSC and CTRP pharmacogenomic data, and a Sparkle spatial transcriptomic section. SHC2-associated transcriptional programs were examined in TCGA-COAD, and loss-of-function experiments were performed in HCT116 and RKO cells.
SHC2 showed heterogeneous expression across cancers. COAD was prioritized because tumor-associated upregulation coincided with stage-related differences and consistently unfavorable survival associations. Genomic, methylation, immune, and drug-response analyses provided context-dependent correlates rather than a uniform pan-cancer pattern. In a COAD spatial section, SHC2 expression colocalized with malignant regions. SHC2-high COAD tumors were enriched for Wnt/β-catenin, TGF-β, and angiogenesis signatures, whereas SHC2 knockdown reduced proliferation, colony formation, migration, and invasion in both cell models.
Convergent computational and in vitro evidence supports SHC2 as a potential prognostic biomarker and candidate regulator of malignant phenotypes in COAD. Causal mechanisms, clinical performance, and therapeutic relevance require validation in independent cohorts, rescue or overexpression systems, and in vivo models.
The findings define a COAD-centered, hypothesis-generating framework in which SHC2 expression is linked to adverse clinical features and tumor-promoting cellular behavior, while avoiding causal interpretation of the correlative pan-cancer analyses.
PMID:
43023365
Bibliographic data and abstract were imported from PubMed on 13 Nov 2026.
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