Evidence map›Paper›PMID 33468994›Full record

ArticleCell death & disease2021

Autophagy augments the self-renewal of lung cancer stem cells by the degradation of ubiquitinated p53.

Jianyu Wang, Doudou Liu, Zhiwei Sun, Ting Ye, Jingyuan Li, Bin Zeng, Qiting Zhao, H Rosie Xing

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Review
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  10. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
  11. Article
  12. Article
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  14. Article
  15. Article
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  18. Article
  19. Review
  20. A perspective on the role of autophagy in cancer.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
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

8 authors at 2 institutions in 1 country.

Jianyu WangInstitute of Life Sciences, Chongqing Medical University, Chongqing, China. wjy2003123@163.com.
Doudou LiuInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Zhiwei SunInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Ting YeInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Jingyuan LiInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Bin ZengInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Qiting ZhaoInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
H Rosie XingState Key Laboratory of Ultrasound Engineering in Medicine Co-Founded by Chongqing and the Ministry of Science and Technology, School of Biomedical Engineering, Chongqing Medical University, Chongqing, China. xinglab310@163.com.ORCID 0000-0001-5894-0837
Chongqing Medical University · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been postulated that cancer stem cells (CSCs) are involved in all aspects of human cancer, although the mechanisms governing the regulation of CSC self-renewal in the cancer state remain poorly defined. In the literature, both the pro- and anti-oncogenic activities of autophagy have been demonstrated and are context-dependent. Mounting evidence has shown augmentation of CSC stemness by autophagy, yet mechanistic characterization and understanding are lacking. In the present study, by generating stable human lung CSC cell lines with the wild-type TP53 (A549), as well as cell lines in which TP53 was deleted (H1229), we show, for the first time, that autophagy augments the stemness of lung CSCs by degrading ubiquitinated p53. Furthermore, Zeb1 is required for TP53 regulation of CSC self-renewal. Moreover, TCGA data mining and analysis show that Atg5 and Zeb1 are poor prognostic markers of lung cancer. In summary, this study has elucidated a new CSC-based mechanism underlying the oncogenic activity of autophagy and the tumor suppressor activity of p53 in cancer, i.e., CSCs can exploit the autophagy-p53-Zeb1 axis for self-renewal, oncogenesis, and progression.

Indexed as

A549 CellsAnimalsAutophagyHeterograftsHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeNeoplastic Stem CellsTumor Suppressor Protein p53UbiquitinationTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33468994
PMCPMC7815724
OpenAlexW3122458786

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.