Evidence map›Paper›PMID 36429016›Full record

ArticleCells2022

A Novel TP53 Gene Mutation Sustains Non-Small Cell Lung Cancer through Mitophagy.

Yuanli Wang, Kah Yong Goh, Zhencheng Chen, Wen Xing Lee, Sze Mun Choy, Jia Xin Fong, Yun Ka Wong, Dongxia Li, Fangrong Hu, Hong-Wen Tang

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  4. Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  14. The Importance of mTORC1-Autophagy Axis for Skeletal Muscle Diseases.International journal of molecular sciences · 2022
    Review
  15. Article
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

10 authors at 3 institutions in 2 countries.

Yuanli WangSchool of Life and Environmental Sciences, Guilin University of Electronic Technology, Guilin 541014, China.
Kah Yong GohProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.
Zhencheng ChenSchool of Life and Environmental Sciences, Guilin University of Electronic Technology, Guilin 541014, China.
Wen Xing LeeProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.
Sze Mun ChoyProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.
Jia Xin FongProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.
Yun Ka WongProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.
Dongxia LiSchool of Electronic Engineering and Automation, Guilin University of Electronic Technology, Guilin 541004, China.
Fangrong HuSchool of Electronic Engineering and Automation, Guilin University of Electronic Technology, Guilin 541004, China.
Hong-Wen TangProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore 169857, Singapore.ORCID 0000-0002-8347-9891
Duke-NUS Medical School · SGGuilin University of Electronic Technology · CNBeibu Gulf University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer death in the world. In particular, non-small-cell lung cancer (NSCLC) represents the majority of the lung cancer population. Advances in DNA sequencing technologies have significantly contributed to revealing the roles, functions and mechanisms of gene mutations. However, the driver mutations that cause cancers and their pathologies remain to be explored. Here, we performed next-generation sequencing (NGS) on tumor tissues isolated from 314 Chinese NSCLC patients and established the mutational landscape in NSCLC. Among 656 mutations, we identified TP53-p.Glu358Val as a driver mutation in lung cancer and found that it activates mitophagy to sustain cancer cell growth. In support of this finding, mice subcutaneously implanted with NSCLC cells expressing TP53-p.Glu358Val developed larger tumors compared to wild-type cells. The pharmaceutical inhibition of autophagy/mitophagy selectively suppresses the cell proliferation of TP53-null or TP53-p.Glu358Val-expressing lung cancer cells. Together, our study characterizes a new TP53 mutation identified from Chinese lung cancer patients and uncovers its roles in regulating mitophagy, providing a new insight into NSCLC treatment.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsGenes, p53HumansMiceMitophagyMutationTumor Suppressor Protein p53Tumor Suppressor Protein p53lung cancermitophagyNSCLCTP53

Identifiers

PMID36429016
PMCPMC9688643
OpenAlexW4309010231

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.