Evidence map›Paper›PMID 25605008›Full record

ArticleOncotarget2015

Metformin inhibits tumor growth by regulating multiple miRNAs in human cholangiocarcinoma.

Xingming Jiang, Ning Ma, Dayong Wang, Fuyuan Li, Rongzhang He, Dongliang Li, Ruiqi Zhao, Qingxin Zhou, Yimin Wang, Fumin Zhang and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

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  15. The Vital Roles of LINC00662 in Human Cancers.Frontiers in cell and developmental biology · 2021
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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

14 authors at 2 institutions in 1 country.

Xingming JiangDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ning MaDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Dayong WangDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Fuyuan LiCenter for Endemic Disease Control, Harbin Medical University, Harbin, China.
Rongzhang HeDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Dongliang LiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Ruiqi ZhaoDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Qingxin ZhouDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yimin WangDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Fumin ZhangDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ming WanDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Pengcheng KangDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xu GaoDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Yunfu CuiDepartment of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antidiabetic drug metformin exerts antineoplastic effects in many types of malignancies, however the effect of metformin on cholangiocarcinoma (CCA) still remains unclear. In the present study, we investigated that metformin treatment was closely associated with the clinicopathologic characteristics and improved postoperative survival of CCA patients. Metformin inhibited CCA tumor growth by cell cycle arrest in vitro and in vivo. We explored that the expression of six miRNAs (mir124, 182, 27b, let7b, 221 and 181a), which could directly target cell-cycle-regulatory genes, was altered by metformin in vitro and in vivo. These miRNAs were dysregulated in cholangiocarcinoma and promoted the CCA genesis and metformin exactly modulated these carcinogenic miRNAs expression to arrest the cell cycle and inhibit the proliferation. Meanwhile, these miRNAs expression changes correlated with the tumor volume and postoperative survival of CCA patients and could be used to predict the prognosis. Further we confirmed that metformin upregulated Drosha to modulate these miRNAs expression. Our results elucidated that metformin inhibited CCA tumor growth via the regulation of Drosha-mediated multiple carcinogenic miRNAs expression and comprehensive evaluation of these miRNAs expression could be more efficient to predict the prognosis. Moreover, metformin might be a quite promising strategy for CCA prevention and treatment.

Indexed as

AnimalsAntineoplastic AgentsBile Duct NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationCholangiocarcinomaDose-Response Relationship, DrugFemaleGene Expression Regulation, NeoplasticHumansHypoglycemic AgentsKaplan-Meier EstimateMetforminMice, NudeMicroRNAsAntineoplastic AgentsDROSHA protein, humanHypoglycemic AgentsMetforminMicroRNAsRibonuclease III

Identifiers

PMID25605008
PMCPMC4413646
OpenAlexW1845565209

What OpenQuestion holds

Textmetadata
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.