Evidence map›Paper›PMID 33767588›Full record

ArticleInternational journal of biological sciences2021

miR-26b enhances the sensitivity of hepatocellular carcinoma to Doxorubicin via USP9X-dependent degradation of p53 and regulation of autophagy.

Enjiang Chen, Enliang Li, Hao Liu, Yue Zhou, Liang Wen, Jianxin Wang, Yi Wang, Longyun Ye, Tingbo Liang

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  6. Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025
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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 at 6 institutions in 1 country.

Enjiang ChenThe Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, China.
Enliang LiDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Hao LiuDepartment of Medical Oncology, Tongde hospital of Zhejiang Province, Hangzhou, Zhejiang, 310012, China.
Yue ZhouDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Liang WenDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jianxin WangDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yi WangZhejiang Provincial Key Laboratory of Pancreatic Disease, Hangzhou, China.
Longyun YeDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Tingbo LiangZhejiang Provincial Key Laboratory of Pancreatic Disease, Hangzhou, China.
Zhejiang University · CNTongde Hospital of Zhejiang Province · CNFirst Affiliated Hospital Zhejiang University · CNFudan University Shanghai Cancer Center · CNSecond Affiliated Hospital of Zhejiang University · CNZhejiang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multi-drug resistance is a major challenge to hepatocellular carcinoma (HCC) treatment, and the over-expression or deletion of microRNA (miRNA) expression is closely related to the drug-resistant properties of various cell lines. However, the underlying molecular mechanisms remain unclear. CCK-8, EdU, flow cytometry, and transmission electron microscopy were performed to determine cell viability, proliferation, apoptosis, autophagic flow, and nanoparticle characterization, respectively. In this study, the results showed that the expression of miR-26b was downregulated following doxorubicin treatment in human HCC tissues. An miR-26b mimic enhanced HCC cell doxorubicin sensitivity, except in the absence of p53 in Hep3B cells. Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment. Tenovin-1 (an MDM2 inhibitor) protected p53 from ubiquitination-mediated degradation only in HepG2 cells with wild type p53. Tenovin-1 pretreatment enhanced HCC cell resistance to doxorubicin when transfected with an miR-26b mimic. Moreover, the miR-26b mimic inhibited doxorubicin-induced autophagy and the autophagy inducer, rapamycin, eliminated the differences in the drug sensitivity effect of miR-26b.

Indexed as

AnimalsAntibiotics, AntineoplasticAutophagyCarcinoma, HepatocellularDoxorubicinDrug Resistance, NeoplasmHep G2 CellsHumansLiver NeoplasmsMiceMice, Inbred BALB CMicroRNAsTumor Suppressor Protein p53Ubiquitin ThiolesteraseXenograft Model Antitumor AssaysAntibiotics, AntineoplasticDoxorubicinMicroRNAsMIRN26 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53Ubiquitin ThiolesteraseUSP9X protein, humanDoxorubicinhepatocellular carcinomamicroRNA-26bp53.USP9X

Identifiers

PMID33767588
PMCPMC7975695
OpenAlexW3131471395

What OpenQuestion holds

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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.