Cytochrome c oxidase subunit VIc (COX6c) is one of the key subunits of the terminal enzyme in the mitochondrial respiratory chain. It plays a crucial role in regulating oxidative phosphorylation (OXPHOS) and energy production within mitochondria. The release of COX6c from mitochondria may mark the onset of the intrinsic apoptosis pathway. Also, its expression changes are associated with various diseases, making it a potential biomarker for diagnosis and treatment [1].

In lung adenocarcinoma, knockdown of COX6C significantly inhibits cell proliferation, induces cell cycle arrest, mitosis deficiency, and apoptosis, and impairs mitochondrial fusion and oxidative phosphorylation [2]. In myocardial infarction, the expression of COX6C was elevated, and methylprotodioscin treatment could decline its expression, reducing oxidative stress and suppressing inflammation [3]. In missed abortion, COX6C was dramatically down-regulated, and its knockdown inhibited apoptosis in relevant cells, suggesting a protective effect [4].

In summary, COX6c is essential for mitochondrial-related functions like OXPHOS and apoptosis. Through model-based research, its roles in diseases such as lung adenocarcinoma, myocardial infarction, and missed abortion have been revealed. These findings contribute to understanding disease mechanisms and may offer new directions for disease treatment and prevention.

References:

1. Wang, Changyu, Lv, Jianjun, Xue, Chengxu, Yang, Yang, Zhang, Shaofei. 2022. Novel role of COX6c in the regulation of oxidative phosphorylation and diseases. In Cell death discovery, 8, 336. doi:10.1038/s41420-022-01130-1. https://pubmed.ncbi.nlm.nih.gov/35879322/

2. Liu, Shuanghui, Shao, Fanggui, Wang, Yourong, Jiang, Hao, Dong, Zhixiong. 2024. COX6C expression driven by copy amplification of 8q22.2 regulates cell proliferation via mediation of mitosis by ROS-AMPK signaling in lung adenocarcinoma. In Cell death & disease, 15, 74. doi:10.1038/s41419-024-06443-w. https://pubmed.ncbi.nlm.nih.gov/38242874/

3. Xu, Zhihui, Song, Tingyu, Yang, Xiufang, Gao, Meng, Xu, Lina. 2024. TMT-based proteomics reveals methylprotodioscin alleviates oxidative stress and inflammation via COX6C in myocardial infraction. In Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 180, 117489. doi:10.1016/j.biopha.2024.117489. https://pubmed.ncbi.nlm.nih.gov/39321507/

4. Chen, Xia, Zheng, Qianwen, Ji, Li, Zheng, Yanli, Yu, Jun. 2022. Quantitative proteomics and functional analysis identified novel targets for missed abortion. In Experimental cell research, 417, 113216. doi:10.1016/j.yexcr.2022.113216. https://pubmed.ncbi.nlm.nih.gov/35605648/