Evidence map›Paper›PMID 25849943›Full record

ArticleOncotarget2015

MicroRNA-3127 promotes cell proliferation and tumorigenicity in hepatocellular carcinoma by disrupting of PI3K/AKT negative regulation.

Jianxin Jiang, Yi Zhang, Yuting Guo, Chao Yu, Meiyuan Chen, Zhu Li, Se Tian, Chengyi Sun

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 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Clinicopathological implications of miR-3127 in melanoma.Journal of pathology and translational medicine · 2025
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  11. Aging · 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

8 authors at 2 institutions in 1 country.

Jianxin JiangDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Yi ZhangZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, China.
Yuting GuoDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Chao YuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Meiyuan ChenDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Zhu LiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Se TianDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Chengyi SunDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, Guiyang, China.
Nanyang Medical College · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that multiple phosphatases deactivate the PI3K/AKT signaling pathway. Here we demonstrated that, by suppressing multiple phosphatases, miR-3127 promotes growth of hepatocellular carcinoma (HCC). Our study also reveals clinical significance of miR-3127 expression in HCC patients. MiR-3127 expression was markedly upregulated in HCC tissues and cells. Furthermore, high miR-3127 expression was associated with an aggressive phenotype and poor prognosis. MiR-3127 overexpression promoted HCC cell proliferation in vitro and tumor growth in vivo. Also, miR-3127 accelerated G1-S transition by activating AKT/ FOXO1 signaling, by directly targeting the 3' untranslated regions (3`UTR) of pleckstrin homology domain leucine-rich repeat protein phosphatase 1/2 (PHLPP1/2), inositol polyphosphate phosphatase 4A (INPP4A), and inositol polyphosphate-5-phosphatase J (INPP5J) mRNA, repressing their expression. In agreement, the miRNA antagonist antagomir-3127 suppressed HCC cell proliferation and tumor growth by inhibiting the AKT/FOXO1 signaling. Taken together, these findings suggest that silencing miR-3127 might be a potential therapeutic strategy.

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularCell Line, TumorCell ProliferationHep G2 CellsHeterograftsHumansLiver NeoplasmsMiceMice, Inbred BALB CMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTransfectionMicroRNAsMIRN3127 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akthepatocellular carcinomaINPP4AmiR-3127PHLPPPI3K/AKT pathway

Identifiers

PMID25849943
PMCPMC4467442
OpenAlexW2124258353

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.