Evidence map›Paper›PMID 31663688›Full record

ArticleCancer medicine2019

COX7A1 suppresses the viability of human non-small cell lung cancer cells via regulating autophagy.

Lei Zhao, Xin Chen, Yetong Feng, Guangsuo Wang, Imran Nawaz, Lifu Hu, Pengfei Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Analysis of Nuclear Encoded Mitochondrial Gene Networks in Cervical Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Lei ZhaoDepartment of Anesthesiology, The 2nd Clinical Medical College (Shenzhen People's Hospital) of Jinan University, The 1st Affiliated Hospitals of Southern University of Science and Technology, Shenzhen, China.
Xin ChenDepartment of Laboratory Medicine, The 2nd Clinical Medicine College (Shenzhen People's Hospital) of Jinan University, The 1st Affiliated Hospitals of Southern University of Science and Technology, Shenzhen, China.
Yetong FengDepartment of Medicine, College of Medicine, University of Arizona, Tucson, AZ, USA.
Guangsuo WangDepartment of Thoracic Surgery, The 2nd Clinical Medicine College (Shenzhen People's Hospital) of Jinan University, The 1st Affiliated Hospitals of Southern University of Science and Technology, Shenzhen, China.
Imran NawazDepartment of Thoracic Surgery, The 2nd Clinical Medicine College (Shenzhen People's Hospital) of Jinan University, The 1st Affiliated Hospitals of Southern University of Science and Technology, Shenzhen, China.
Lifu HuDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Pengfei LiuDepartment of Anesthesiology, The 2nd Clinical Medical College (Shenzhen People's Hospital) of Jinan University, The 1st Affiliated Hospitals of Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0003-0172-189X
Jinan University · CNKarolinska Institutet · SEUniversity of Arizona · US

Funding

China Postdoctoral Science Foundation 2019M653277National Natural Science Foundation of China 31900547Science and Technology Planning Project of Guangdong Province 2016ZC0244Shenzhen Peacock Plan KQTD2016113015442590
6 · The paper itself

Abstract

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.

Indexed as

ApoptosisAutophagosomesAutophagyCarcinoma, Non-Small-Cell LungCell Line, TumorCell SurvivalElectron Transport Complex IVGene ExpressionHumansLung NeoplasmsNADPH Oxidase 2RNA, Small InterferingCOX7A1 protein, humanCYBB protein, humanElectron Transport Complex IVNADPH Oxidase 2RNA, Small Interferingautophagycell viabilityCOX7A1non-small cell lung cancerNOX2PGC-1α

Identifiers

PMID31663688
PMCPMC6912042
OpenAlexW2982689058

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.