COX7A1 suppresses the viability of human non-small cell lung cancer cells via regulating autophagy
| Autor: | Imran Nawaz, Pengfei Liu, Guangsuo Wang, Li-Fu Hu, Lei Zhao, Xin Chen, Yetong Feng |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Autophagosome non‐small cell lung cancer Cancer Research autophagy Lung Neoplasms Cell Survival Gene Expression Apoptosis COX7A1 lcsh:RC254-282 Electron Transport Complex IV 03 medical and health sciences 0302 clinical medicine NOX2 Downregulation and upregulation Carcinoma Non-Small-Cell Lung Cell Line Tumor PGC‐1α Humans Radiology Nuclear Medicine and imaging Viability assay RNA Small Interfering cell viability Original Research Cancer Biology Chemistry Cell growth Autophagy Autophagosomes Transfection lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cell biology 030104 developmental biology Mitochondrial respiratory chain Oncology 030220 oncology & carcinogenesis NADPH Oxidase 2 |
| Zdroj: | Cancer Medicine Cancer Medicine, Vol 8, Iss 18, Pp 7762-7773 (2019) |
| ISSN: | 2045-7634 |
| Popis: | COX7A1 is a subunit of cytochrome c oxidase, and plays an important role in the super‐assembly that integrates peripherally into multi‐unit heteromeric complexes in the mitochondrial respiratory chain. In recent years, some researchers have identified that COX7A1 is implicated in human cancer cell metabolism and therapy. In this study, we mainly explored the effect of COX7A1 on the cell viability of lung cancer cells. COX7A1 overexpression was induced by vector transfection in NCI‐H838 cells. Cell proliferation, colony formation and cell apoptosis were evaluated in different groups. In addition, autophagy was analyzed by detecting the expression level of p62 and LC3, as well as the tandem mRFP‐GFP‐LC3 reporter assay respectively. Our results indicated that the overexpression of COX7A1 suppressed cell proliferation and colony formation ability, and promoted cell apoptosis in human non‐small cell lung cancer cells. Besides, the overexpression of COX7A1 blocked autophagic flux and resulted in the accumulation of autophagosome via downregulation of PGC‐1α and upregulation of NOX2. Further analysis showed that the effect of COX7A1 overexpression on cell viability was partly dependent of the inhibition of autophagy. Herein, we identified that COX7A1 holds a key position in regulating the development and progression of lung cancer by affecting autophagy. Although the crosstalk among COX7A1, PGC‐1α and NOX2 needs further investigation, our study provides a novel insight into the therapeutic action of COX7A1 against human non‐small cell lung cancer. COX7A1 could inhibit cell proliferation and colony formation ability, as well as promote cancer cell apoptosis. COX7A1 overexpression blocked the autophagic flux via downregulation of PGC‐1α and upregulation of NOX2. |
| Databáze: | OpenAIRE |
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