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COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy
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 m...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912042/ https://www.ncbi.nlm.nih.gov/pubmed/31663688 http://dx.doi.org/10.1002/cam4.2659 |
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author | Zhao, Lei Chen, Xin Feng, Yetong Wang, Guangsuo Nawaz, Imran Hu, Lifu Liu, Pengfei |
author_facet | Zhao, Lei Chen, Xin Feng, Yetong Wang, Guangsuo Nawaz, Imran Hu, Lifu Liu, Pengfei |
author_sort | Zhao, Lei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6912042 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-69120422019-12-23 COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy Zhao, Lei Chen, Xin Feng, Yetong Wang, Guangsuo Nawaz, Imran Hu, Lifu Liu, Pengfei Cancer Med Cancer Biology 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. John Wiley and Sons Inc. 2019-10-30 /pmc/articles/PMC6912042/ /pubmed/31663688 http://dx.doi.org/10.1002/cam4.2659 Text en © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Cancer Biology Zhao, Lei Chen, Xin Feng, Yetong Wang, Guangsuo Nawaz, Imran Hu, Lifu Liu, Pengfei COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title | COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title_full | COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title_fullStr | COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title_full_unstemmed | COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title_short | COX7A1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
title_sort | cox7a1 suppresses the viability of human non‐small cell lung cancer cells via regulating autophagy |
topic | Cancer Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912042/ https://www.ncbi.nlm.nih.gov/pubmed/31663688 http://dx.doi.org/10.1002/cam4.2659 |
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