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COX7A2L drives lung adenocarcinoma progression and radioresistance via PI3K/AKT signaling
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DOI：10.1016/j.lfs.2026.124607.png)
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Abstract
En 中文
Radioresistance poses a significant challenge in lung adenocarcinoma (LUAD) treatment, and the role of mitochondrial regulation in this process remains poorly understood. This study investigated the function of the mitochondria-associated protein COX7A2L in LUAD progression and radioresistance. We integrated multi-omics analyses, including bulk, single-cell, and spatial transcriptomics, with in vitro and in vivo functional experiments using COX7A2L knockdown and overexpression models. Our results demonstrated that COX7A2L was significantly upregulated in LUAD tissues and correlated with poor patient prognosis. Functionally, COX7A2L promoted cancer cell proliferation, migration, and invasion, and conferred radioresistance by enhancing DNA damage repair. Mechanistically, COX7A2L expression was associated with altered reactive oxygen species (ROS) levels and activation of the PI3K/AKT signaling pathway. Pharmacological inhibition of PI3K/AKT signaling attenuated the malignant phenotypes and radioresistant effects associated with COX7A2L, suggesting that PI3K/AKT signaling may contribute to COX7A2L-mediated LUAD progression and radioresistance. Collectively, our findings identify COX7A2L as a potential driver of LUAD malignancy and radioresistance and highlight COX7A2L as a promising therapeutic target for radiosensitization in LUAD.
Keywords:
LUAD
Radioresistance
COX7A2L
PI3K-AKT signaling
ROS
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