
msiCAT-tailing은 ATP5α 단백질의 기능을 변화시켜 미토콘드리아 막전위를 증가시키고 MPTP 개방을 억제함으로써 신경교종 세포의 생존, 이동 및 약물 저항성을 높인다.


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The rapid and sustained proliferation in cancer cells requires accelerated protein synthesis. Accelerated protein synthesis and disordered cell metabolism in cancer cells greatly increase the risk of translation errors. ribosome-associated quality control (RQC) is a recently discovered mechanism for resolving ribosome collisions caused by frequent translation stalls. The role of the RQC pathway in cancer initiation and progression remains controversial and confusing. In this study, we investigated the pathogenic role of mitochondrial stress-induced protein carboxyl-terminal terminal alanine and threonine tailing (msiCAT-tailing) in glioblastoma (GBM), which is a specific RQC response to translational arrest on the outer mitochondrial membrane. We found that msiCAT-tailed mitochondrial proteins frequently exist in glioblastoma stem cells (GSCs). Ectopically expressed msiCAT-tailed mitochondrial ATP synthase F1 subunit alpha (ATP5α) protein increases the mitochondrial membrane potential and blocks mitochondrial permeability transition pore (MPTP) formation/opening. These changes in mitochondrial properties confer resistance to staurosporine (STS)-induced apoptosis in GBM cells. Therefore, msiCAT-tailing can promote cell survival and migration, while genetic and pharmacological inhibition of msiCAT-tailing can prevent the overgrowth of GBM cells.

Highlights 

### Competing Interest Statement

The authors have declared no competing interest.

The mitochondrial stress-induced protein carboxyl-terminal alanine and threonine tailing (msiCAT-tailing) promotes glioblastoma tumorigenesis by modulating mitochondrial functions

신경교종-발생에-기여하는-미토콘드리아-스트레스-유도-단백질-카복실-말단-알라닌-및-트레오닌-부가-msicat-tailing-기전


신경교종 발생에 기여하는 미토콘드리아 스트레스 유도 단백질 카복실 말단 알라닌 및 트레오닌 부가(msiCAT-tailing) 기전
