Evidence map›Paper›PMID 32631421›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

Metformin inhibits cervical cancer cell proliferation by modulating PI3K/Akt-induced major histocompatibility complex class I-related chain A gene expression.

Chenglai Xia, Chang Liu, Zhihong He, Yantao Cai, Jinman Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Depletion of the RNA-Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Metabolic mechanisms of immunotherapy resistance.Exploration of targeted anti-tumor therapy · 2025
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  13. Cancers · 2024
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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 at 1 institution in 1 country.

Chenglai XiaSouth Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China. xiachenglai@126.com.ORCID http://orcid.org/0000-0002-4528-7960
Chang LiuSouth Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China.
Zhihong HeSouth Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China.
Yantao CaiSouth Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China.
Jinman ChenSouth Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China.
Foshan Maternity and Child Health Care Hospital · CN

Funding

Foshan Medicine Dengfeng Project of China 2019-2021
6 · The paper itself

Abstract

backgroundRecent studies have shown that the classic hypoglycemic drug metformin inhibits tumor growth; however, the underlying mechanism remains unclear. We previously showed that metformin disrupts the sponge effect of long non-coding RNA MALAT1/miR-142-3p to inhibit cervical cancer cell proliferation. In this study, we interrogated the ability of metformin to modulate the anti-tumor immune response in cervical cancer.

methodsThe cell counting kit-8 assay was used to detect the viability of cervical cancer cells. Flow cytometry assays were performed to measure cell apoptosis and cell cycle. Lactate dehydrogenase (LDH) cytotoxicity assay was used to detect NK Cell Cytotoxicity. Relative protein levels were determined by immunoblotting and relative gene levels were determined by quantitative real-time PCR. Tumor Xenograft Modeling was used to evaluate the effect of metformin in vivo.

resultsMetformin inhibited cervical cancer cell proliferation, cervical cancer xenograft growth, expression of PCNA, p-PI3K and p-Akt. Moreover metformin induced cervical cancer cell apoptosis and caused cancer cell cycle arrest. In addition, metformin upregulated the expression of DDR-1 and p53 in human cervical cancer cells. Furthermore, metformin also regulated the mRNA and protein expression of MICA and HSP70 on the surface of human cervical cancer cells via the PI3K/Akt pathway, enhancing NK cell cytotoxicity.

conclusionsIn conclusion, our results suggest that metformin may be used as immunopotentiator to inhibit cervical cancer progression and may be considered a viable candidate for combination therapy with immunotherapy.

Indexed as

AnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IHumansHypoglycemic AgentsMetforminMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBiomarkers, TumorHistocompatibility Antigens Class IHypoglycemic AgentsMetforminPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCell proliferationCervical cancerHistocompatibility complex class I-related chain aMetforminPI3K

Identifiers

PMID32631421
PMCPMC7336474
OpenAlexW3039977220

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.