Evidence map›Paper›PMID 33854041›Full record

ArticleCell death & disease2021

Sirt1 deacetylates and stabilizes p62 to promote hepato-carcinogenesis.

Lifeng Feng, Miaoqin Chen, Yiling Li, Muchun Li, Shiman Hu, Bingluo Zhou, Liyuan Zhu, Lei Yu, Qiyin Zhou, Linghui Tan and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Review
  8. NBR1-Mediated Autophagic Degradation of YTHDF1 CurtailsCancer communications (London, England) · 2026
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Reversible Acetylation of Non-histone Proteins in Human Cancers.Results and problems in cell differentiation · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. 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

13 authors at 1 institution in 1 country.

Lifeng Feng *Laboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.ORCID 0000-0003-4506-1213
Miaoqin Chen *Laboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Yiling LiLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Muchun LiLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Shiman HuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Bingluo ZhouLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Liyuan ZhuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.ORCID 0000-0001-6959-9435
Lei YuLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Qiyin ZhouLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Linghui TanLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China.
Huimin AnDepartment of Pathology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Xian WangDepartment of Medical Oncology, Key lab of Biotherapy in Zhejiang, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Hongchuan JinLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Institute of Zhejiang University, Sir Run Run Shaw hospital, School of Medicine, Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China. jinhc@zju.edu.cn.ORCID 0000-0002-6697-3097
Sir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p62/SQSTM1 is frequently up-regulated in many cancers including hepatocellular carcinoma. Highly expressed p62 promotes hepato-carcinogenesis by activating many signaling pathways including Nrf2, mTORC1, and NFκB signaling. However, the underlying mechanism for p62 up-regulation in hepatocellular carcinoma remains largely unclear. Herein, we confirmed that p62 was up-regulated in hepatocellular carcinoma and its higher expression was associated with shorter overall survival in patients. The knockdown of p62 in hepatocellular carcinoma cells decreased cell growth in vitro and in vivo. Intriguingly, p62 protein stability could be reduced by its acetylation at lysine 295, which was regulated by deacetylase Sirt1 and acetyltransferase GCN5. Acetylated p62 increased its association with the E3 ligase Keap1, which facilitated its poly-ubiquitination-dependent proteasomal degradation. Moreover, Sirt1 was up-regulated to deacetylate and stabilize p62 in hepatocellular carcinoma. Additionally, Hepatocyte Sirt1 conditional knockout mice developed much fewer liver tumors after Diethynitrosamine treatment, which could be reversed by the re-introduction of exogenous p62. Taken together, Sirt1 deacetylates p62 at lysine 295 to disturb Keap1-mediated p62 poly-ubiquitination, thus up-regulating p62 expression to promote hepato-carcinogenesis. Therefore, targeting Sirt1 or p62 is a reasonable strategy for the treatment of hepatocellular carcinoma.

Indexed as

AnimalsAutophagyCarcinogenesisCarcinoma, HepatocellularKelch-Like ECH-Associated Protein 1Liver NeoplasmsMiceMice, Inbred BALB CProtein Processing, Post-TranslationalSignal TransductionSirtuin 1Kelch-Like ECH-Associated Protein 1Sirt1 protein, mouseSirtuin 1

Identifiers

PMID33854041
PMCPMC8046979
OpenAlexW3155781726

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.