Evidence map›Paper›PMID 28045889›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Metformin Induces Growth Inhibition and Cell Cycle Arrest by Upregulating MicroRNA34a in Renal Cancer Cells.

Wei Xie, Lei Wang, Halei Sheng, Jing Qiu, Di Zhang, Le Zhang, Fan Yang, Dahai Tang, Kebin Zhang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Dissecting the role of metformin in urogenital malignancies.Annals of medicine and surgery (2012) · 2025
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  20. Activation of AMP-activated protein kinase during sepsis/inflammation improves survival by preserving cellular metabolic fitness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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 3 institutions in 1 country.

Wei XieCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Lei WangCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Halei ShengCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Jing QiuCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Di ZhangCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Le ZhangCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Fan YangCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Dahai TangDepartment of Laboratory Medicine, No.411 Hospital of CPLA, Shanghai, China (mainland).
Kebin ZhangCentral Laboratory, Xinqiao Hospital, Third Military Medical University, Chongqing, China (mainland).
Xinqiao Hospital · CNArmy Medical University · CNPeople's Liberation Army 411 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Metformin is a widely used biguanide drug for the treatment of type 2 diabetes. It has been revaluated as a potential anti-cancer drug with promising activity in various tumors. However, the precise mechanisms underlying the suppression of cancer cells by metformin remain not well understood. MATERIAL AND METHODS In this study, human renal cell carcinoma cell line ACHN was used to investigate the anti-proliferation effect of metformin. A cell counting kit-8 assay was used to detect the cell viability. The cell cycle distribution and apoptosis were analyzed by flow cytometry. The expression of cyclin D1 and p27KIP1 was detected by Western blot. The underlying mechanism involving miRNA34a was further investigated by quantitative RT-PCR and transfection with miRNA inhibitor specific for miRNA34a in ACHN, 769-P, and A498 cells. RESULTS Metformin could significantly inhibit the proliferation of ACHN cells in a dose- and time-dependent manner. In addition, the results showed that metformin induced G0/G1 phase arrest and delayed entry into S phase in ACHN cells. It was shown that metformin downregulates the expression of cyclin D1 and increases the p27KIP1 level. Furthermore, metformin increased ACHN cell death. Lastly, miRNA34a was found to be upregulated by metformin in ACHN, 769-P, and A498 cells. Subsequently, it was demonstrated that inhibition of miRNA34a could partially attenuate the suppressive effect of metformin on renal cancer cell proliferation. CONCLUSIONS The study data revealed that metformin induced cell growth inhibition and cell cycle arrest partially by upregulating miRNA34a in renal cancer cells.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, Renal CellCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalHumansKidney NeoplasmsMetforminMicroRNAsUp-RegulationAntineoplastic AgentsMetforminMicroRNAsMIRN34 microRNA, human

Identifiers

PMID28045889
PMCPMC5226302
OpenAlexW2565733578

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.