Evidence map›Paper›PMID 38045832›Full record

ArticleMedComm2023

Ubiquitin-specific protease 22 promotes tumorigenesis and progression by an FKBP12/mTORC1/autophagy positive feedback loop in hepatocellular carcinoma.

Qianwei Ye, Wei Zhou, Shengjun Xu, Qingyang Que, Qifan Zhan, Lincheng Zhang, Shusen Zheng, Sunbin Ling, Xiao Xu

Abstract read
In one paragraph

Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Role of the USP family in autophagy regulation and cancer progression.Apoptosis : an international journal on programmed cell death · 2025
    Review
  8. Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025
    Review
  9. Bioinformatic analysis of the role of USP22 expression in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. 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

9 authors.

Qianwei YeDepartment of General Surgery Hangzhou First People's Hospital Hangzhou China.
Wei ZhouZhejiang University School of Medicine Hangzhou China.
Shengjun XuDepartment of General Surgery Hangzhou First People's Hospital Hangzhou China.
Qingyang QueZhejiang University School of Medicine Hangzhou China.
Qifan ZhanZhejiang University School of Medicine Hangzhou China.
Lincheng ZhangZhejiang University School of Medicine Hangzhou China.
Shusen ZhengNHC Key Laboratory of Combined Multi-Organ Transplantation Hangzhou China.
Sunbin LingDepartment of General Surgery Hangzhou First People's Hospital Hangzhou China.
Xiao XuZhejiang University School of Medicine Hangzhou China.ORCID https://orcid.org/0000-0002-2761-2811

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-specific protease 22 (USP22) has been identified as a potential marker for cancer stem cells in hepatocellular carcinoma (HCC). It can promote HCC stemness, which is considered a driver of tumorigenesis. Here, we sought to determine the role of USP22 in tumorigenesis, elucidate its underlying mechanism, and explore its therapeutic significance in HCC. As a result, we found that tissue-specific Usp22 overexpression accelerated tumorigenesis, whereas Usp22 ablation decelerated it in a c-Myc/NRasGV12-induced HCC mouse model and that the mammalian target of rapamycin complex 1 (mTORC1) pathway was activated downstream. USP22 overexpression resulted in increased tumorigenic properties that were reversed by rapamycin in vitro and in vivo. In addition, USP22 activated mTORC1 by deubiquitinating FK506-binding protein 12 (FKBP12) and activated mTORC1, in turn, further stabilizing USP22 by inhibiting autophagic degradation. Clinically, HCC patients with high USP22 expression tend to benefit from mTOR inhibitors after liver transplantation (LT). Our results revealed that USP22 promoted tumorigenesis and progression via an FKBP12/mTORC1/autophagy positive feedback loop in HCC. Clinically, USP22 may be an effective biomarker for selecting eligible recipients with HCC for anti-mTOR-based therapy after LT.

Indexed as

autophagyFK506‐binding protein 12 (FKBP12)hepatocellular carcinoma (HCC)mammalian target of rapamycin complex 1 (mTORC1)tumorigenesisubiquitin‐specific protease 22 (USP22)

Identifiers

PMID38045832
PMCPMC10691294

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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.