Evidence map›Paper›PMID 36119836›Full record

ArticleAmerican journal of cancer research2022

COA3 overexpression promotes non-small cell lung cancer metastasis by reprogramming glucose metabolism.

Hongwei Lin, Yanjun Gao, Kang Sun, Qian Zhang, Yujuan Li, Min Chen, Faguang Jin

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  3. Association of Single-Nucleotide Polymorphisms onInternational journal of molecular sciences · 2025
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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 2 institutions in 1 country.

Hongwei LinDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Yanjun GaoDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Kang SunDepartment of Respiratory and Critical Care Medicine, The 989th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army Luoyang 471000, Henan Province, China.
Qian ZhangDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Yujuan LiDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Min ChenDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Faguang JinDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, The Air Force Medical University Xi'an 710038, Shaanxi Province, China.
Tang Du Hospital · CNPeople's Liberation Army No. 150 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances in cancer research have revealed a close relationship between mitochondrial dysfunction and cancer development. Human COX assembly factor 3 (COA3), also known as CCDC56, is a mitochondrial transmembrane protein responsible for cytochrome c oxidase (COX) protein complex assembly. However, the clinical implication and biological functions of COA3 remain unexplored in human cancers, including non-small cell lung cancer (NSCLC). Here, we found that COA3 is overexpressed at both mRNA and protein levels in human NSCLC cells, mainly as a result of decreased miR-338-3p level. The protein expression level of COA3 is positively associated with lymph node metastasis and predicts poor survival in patients with NSCLC. Silencing of COA3 significantly attenuated, while forced COA3 expression enhanced the migration and invasiveness of NSCLC cells. Mechanistically, we found that aerobic glycolysis, induced at least in part by dynamic-related protein 1 (DRP1) phosphorylation-mediated mitochondrial fragmentation, contributed to COA3-promoted NSCLC metastasis. Together, our study illustrates that COA3 plays a crucial role in NSCLC carcinogenesis, implying COA3 as a prognostic marker and treatment target in NSCLC.

Indexed as

COA3glycolysismetastasismitochondrial fragmentationNSCLC

Identifiers

PMID36119836
PMCPMC9442012
OpenAlexW4296330126

What OpenQuestion holds

Textmetadata
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.