ArticleFrontiers in genetics2026
Multi-omics landscape and functional validation of HCCS in breast cancer: from pan-cancer immunometabolic characterization to regulating tumor proliferation.
Article in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Holocytochrome c synthase (HCCS) is an essential mitochondrial regulator; however, its pan-cancer significance and its direct functional role in breast cancer (BRCA) progression remain insufficiently explored. This study aimed to systematically characterize the pan-cancer landscape of HCCS and validate its biological impact on BRCA. Methods: We integrated multi-omics data from 33 TCGA cancer types to investigate HCCS expression patterns, genomic alterations, and its correlation with the immune microenvironment. In breast cancer cell lines (MDA-MB-231), the effects of HCCS knockdown on cell proliferation and cell cycle distribution were assessed using CCK-8, colony formation, and flow cytometry assays. Finally, we constructed a machine learning-based prognostic signature and performed drug sensitivity analysis to evaluate its clinical relevance. Results: HCCS was significantly upregulated in multiple malignancies, including BRCA, and correlated with poor patient prognosis. Pan-cancer analysis suggested that HCCS might act as a mitochondrial-immunometabolic hub involved in immune evasion. Conclusion: Our findings transition HCCS from a computational biomarker to a functionally validated regulator of breast cancer cell survival. By linking its systemic immunometabolic impact with its direct role in cell cycle control, this study identifies HCCS as a promising therapeutic target and a reliable prognostic indicator in BRCA.
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