Authors
Zikai Xu, Jie Shen, Yizhou Lin, Haotian Shi, Cong Zhang, Zhengwei Zhang, Xiaoyu Zhou, Zheng Yang
Published in
Oncology reports. Volume 56. Issue 6. Epub Oct 16, 2026.
Abstract
Lung adenocarcinoma (LUAD) remains a leading cause of cancer‑related mortality, and mitochondrial proteins have been increasingly implicated in tumor progression. Coiled‑coil‑helix‑coiled‑coil‑helix domain‑containing 2 (CHCHD2) has been reported in several malignancies, yet its pan‑cancer landscape and LUAD‑specific functional relevance have not been comprehensively evaluated. In the present study, multi‑omics analyses were integrated using The Cancer Genome Atlas‑derived datasets and public resources [including Gene Expression Profiling Interactive Analysis (GEPIA) 2, CIBERSORT and CellMiner] to characterize CHCHD2 expression patterns, clinical associations, tumor microenvironment (TME) features, stemness‑related indices and drug‑response correlations across cancers, followed by experimental validation in LUAD models. CHCHD2 was found to be upregulated in multiple cancers and was correlated with advanced disease stage and poor overall survival, especially in patients with LUAD. CHCHD2 promoted cell proliferation and migration while inhibiting apoptosis. CHCHD2 knockdown reduced AKT and ERK phosphorylation and suppressed xenograft tumor growth in vivo. High CHCHD2 expression was associated with increased stemness, an immunosuppressive TME, and differential drug‑response patterns in CellMiner analyses, suggesting that CHCHD2 expression may be associated with compound‑specific sensitivity profiles. Collectively, these findings support an oncogenic role of CHCHD2 in LUAD and highlight its potential utility as a prognostic biomarker and therapeutic target.
PMID:
42885315
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.
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