Evidence map›Paper›PMID 32547320›Full record

ArticleInternational journal of medical sciences2020

AKR1B10 Inhibitor Epalrestat Facilitates Sorafenib-Induced Apoptosis and Autophagy Via Targeting the mTOR Pathway in Hepatocellular Carcinoma.

Nan Geng, Yuanyuan Jin, Yurong Li, Shixuan Zhu, Han Bai

Abstract read
In one paragraph

Article in International journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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  5. Chinese herbal medicines · 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

5 authors.

Nan GengDepartment of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Yuanyuan JinLaboratory of Biomaterials and Translational Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.
Yurong LiDepartment of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Shixuan ZhuDepartment of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Han BaiDepartment of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang 110004, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sorafenib is the standard systemic treatment for advanced hepatocellular carcinoma (HCC), and improving its therapeutic effects is crucial for addressing cancer aggression. We previously reported that epalrestat, an aldo-keto reductase 1B10 inhibitor, enhanced sorafenib's inhibitory effects on HCC xenograft in nude mice. This study aimed to elucidate the mechanism of epalrestat's anti-tumour enhancing effects on sorafenib. HepG2 cells were treated with sorafenib, epalrestat, and their combination. Cell proliferation was assessed with Cell Counting Kit-8 and colony formation assays. AKR1B10 supernate concentration and enzyme activity were detected by ELISA assay and the decrease of optical density of NADPH at 340 nm. Cell cycle and apoptosis analyses were performed with flow cytometry. Western blots clarified the molecular mechanism underlying effects on cell cycle, apoptosis, and autophagy. The anti-tumour mechanism was then validated

Indexed as

Aldo-Keto Reductase Family 1 member B10Antineoplastic Combined Chemotherapy ProtocolsApoptosisAutophagyBlotting, WesternCell Cycle CheckpointsCell SurvivalEnzyme-Linked Immunosorbent AssayFluorescent Antibody TechniqueHep G2 CellsHeterograftsHumansImmunohistochemistryIn Situ Nick-End LabelingRhodanineSorafenibAldo-Keto Reductase Family 1 member B10epalrestatRhodanineSorafenibThiazolidinesTOR Serine-Threonine KinasesAKR1B10apoptosisautophagyhepatocellular carcinomamTOR signalling pathwaysorafenib

Identifiers

PMID32547320
PMCPMC7294918

What OpenQuestion holds

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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.