Evidence map›Paper›PMID 42153130›Full record

ArticleJournal of hepatocellular carcinoma2026

USP9X Promotes Hepatocellular Carcinoma Progression via Stabilization of HSP90AA1.

Hanlin Jiang, Lining Huang, Jiahao Chen, Zongying Jiang, Weiqiao Niu, Jianwu Wu, Zhiming Qiao, Yujia Pan, Xinwei Jiang

Abstract read
In one paragraph

Article in Journal of hepatocellular carcinoma, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Hanlin Jiang *Department of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.ORCID 0009-0001-4430-6197
Lining Huang *Department of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.ORCID 0000-0003-1177-4530
Jiahao Chen *Department of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Zongying JiangDepartment of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Weiqiao NiuDepartment of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Jianwu WuDepartment of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Zhiming QiaoDepartment of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Yujia PanCenter for Scientific Research and Innovation, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.
Xinwei JiangDepartment of Hepatobiliary Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Nanjing Medical University, Suzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. Ubiquitin-specific proteases (USPs) modulate tumor progression by regulating substrate protein stability. However, the mechanisms of most DUBs in HCC remain poorly understood. This study aimed to investigate the role of USP9X in promoting HCC cell proliferation, survival, migration, and invasion. Methods: Transcriptomic and clinical data of LIHC patients were obtained from TCGA to assess USP9X expression, prognosis, and pathway enrichment. USP9X expression in HCC and adjacent tissues was examined by immunohistochemistry and Western blotting. Functional assays (CCK-8, colony formation, wound-healing, Transwell) were performed following USP9X knockdown or overexpression in Lm3 and Huh7 cells. The USP9X-HSP90AA1 interaction was evaluated by Co-IP and mass spectrometry, and deubiquitination assays elucidated the mechanism. In vitro and in vivo experiments determined the effects of USP9X-HSP90AA1 signaling on HCC growth and metastasis. Results: Bioinformatic analyses revealed that USP9X expression was significantly elevated in LIHC tissues and correlated with poor prognosis. Immunohistochemistry and Western blotting confirmed higher USP9X protein levels in tumor tissues. Knockdown of USP9X inhibited proliferation and migration of Lm3 and Huh7 cells, whereas USP9X overexpression enhanced these phenotypes. Co-IP demonstrated a direct interaction between USP9X and HSP90AA1, and deubiquitination assays showed that USP9X decreased HSP90AA1 ubiquitination and increased its stability. Both in vitro and in vivo data indicated that USP9X promotes HCC progression through stabilization of HSP90AA1. Conclusion: USP9X is a tumor-promoting factor that accelerates HCC progression by stabilizing HSP90AA1, highlighting USP9X as a potential therapeutic target for HCC.

Indexed as

bioinformatics translationCO-IPdeubiquitinationHCCHSP90AA1USP9X

Identifiers

PMID42153130
PMCPMC13180381

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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.