Evidence map›Paper›PMID 40170617›Full record

ArticleActa biochimica et biophysica Sinica2025

miR-32-5p suppresses the progression of hepatocellular carcinoma by regulating the GSK3β/NF-κB signaling.

Guangzhi Wang, Qianqian Yang, Yaqi Han, Yunlong Zhang, Wei Pan, Zhongliang Ma, Hui Tian, Xudong Qu

Abstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026
    Article
  3. 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

8 authors.

Guangzhi WangDepartment of Oncology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China.
Qianqian YangLab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai 200444, China.
Yaqi HanLab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai 200444, China.
Yunlong ZhangSchool of Medical Imaging, Shandong Second Medical University, Weifang 261053, China.
Wei PanLab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai 200444, China.
Zhongliang MaLab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai 200444, China.
Hui TianDepartment of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai 200030, China.
Xudong QuDepartment of Intervention Radiology, Zhongshan Hospital, Fudan University, Shanghai 200030, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a highly fatal form of malignancy that seriously threatens patient survival. The global 5-year survival rate for HCC patients ranges from 15% to 19%, and nearly 80% of patients are diagnosed at an advanced stage. Therefore, exploring the mechanism of HCC development and identifying biomarkers and therapeutic targets for HCC are vital. MicroRNAs (miRNAs), a class of noncoding single-stranded RNAs, are 20-24 nucleotides (nt) long. They play pivotal roles in modulating the progression of diverse diseases. The specific role of miR-32-5p in the development of HCC remains unclear. In this study, qRT-PCR is utilized to precisely determine the downregulated expression levels of miR-32-5p in HCC. Subsequently, functional analysis reveals the suppressive role of miR-32-5p in modulating the proliferative and migratory capabilities of HCC cells. Glycogen synthase kinase 3β (GSK3β) has emerged as a potential target of miR-32-5p, which is confirmed through a dual-luciferase reporter assay. Notably, the expression of GSK3β in HCC tissue specimens is negatively correlated with the abundance of miR-32-5p, and patients with high GSK3β expression have shorter survival time. Furthermore, the targeted downregulation of GSK3β remarkably impedes the proliferation and migration of tumor cells. This study suggests that miR-32-5p inhibits the proliferation and migration of HCC through regulating the GSK3β/NF-κB signaling pathway. Therefore, this study reveals that miR-32-5p exerts its suppressive effect on HCC progression, suggesting that it is a promising target for both diagnostic and targeted therapeutic interventions against HCC.

Indexed as

Carcinoma, HepatocellularGlycogen Synthase Kinase 3 betaLiver NeoplasmsMicroRNAsNF-kappa BSignal TransductionCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleGlycogen Synthase Kinase 3 betaGSK3B protein, humanMicroRNAsNF-kappa BGSK3βhepatocellular carcinomamiR-32-5pNF-κB signaling pathway

Identifiers

PMID40170617
PMCPMC12368002

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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.