Evidence map›Paper›PMID 26389681›Full record

ArticleOncotarget2015

MiR-125a suppresses tumor growth, invasion and metastasis in cervical cancer by targeting STAT3.

Zhongyi Fan, Hanzhi Cui, Xiaojie Xu, Zhi Lin, Xuelin Zhang, Lei Kang, Baiyu Han, Jing Meng, Zhifeng Yan, Xiang Yan and 1 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 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

26 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 1 country.

Zhongyi FanDepartment of Oncology, PLA General Hospital, Beijing, China.
Hanzhi CuiDepartment of Oncology, 309th Hospital of PLA, Beijing, China.
Xiaojie XuDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Zhi LinDepartment of Oncology, PLA General Hospital, Beijing, China.
Xuelin ZhangDepartment of Oncology, PLA General Hospital, Beijing, China.
Lei KangDepartment of Nuclear Medicine, Peking University First Hospital, Beijing, China.
Baiyu HanDepartment of Endocrinology and Metablism, 264th Hospital of PLA, Shanxi, China.
Jing MengDepartment of Oncology, PLA General Hospital, Beijing, China.
Zhifeng YanDepartment of Oncology, PLA General Hospital, Beijing, China.
Xiang YanDepartment of Oncology, PLA General Hospital, Beijing, China.
Shunchang JiaoDepartment of Oncology, PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNBeijing VDJBio (China) · CNPeking University · CNThe 309th Hospital of Chinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-125a has been characterized as a tumor suppressor in several cancers. However, the role of miR-125a in cervical cancer is unknown. In this study, we found the expression of miR-125a was downregulated in cervical cancer patients, and negatively correlated with the tumor size, FIGO stage, and preoperative metastasis. Kaplan-Meier analysis showed that miR-125a expression predicted favorable outcome for cervical cancer patients. Dual luciferase assays identified the STAT3 gene as a novel direct target of miR-125a. Functional studies showed that miR-125a overexpression significantly suppressed the growth, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer cells both in vitro and in vivo via decreasing STAT3 expression. Moreover, miR-125a conferred to G2/M cell cycle arrest, accompanied by inhibition of several G2/M checkpoint proteins. Mechanistically, inactivation of miR-125a during cervical carcinogenesis was caused by HPV suppression of p53 expression. Clinically, STAT3, the expression of which, predicted poorer outcome, was inversely correlated with miR-125a in cervical cancer. These data highlight the importance of miR-125a in the cell proliferation and progression of cervical cancer, and indicate that miR-125a may be a useful therapeutic target for cervical cancer.

Indexed as

Cell MovementCell Proliferation3' Untranslated RegionsAdenocarcinomaAnimalsBinding SitesCarcinoma, Squamous CellEpithelial-Mesenchymal TransitionFemaleG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHeLa CellsHumansKaplan-Meier EstimateMice, Inbred BALB CMice, Nude3' Untranslated RegionsMicroRNAsMIRN125 microRNA, humanSTAT3 protein, humanSTAT3 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53cell growthcervical cancermetastasismiR-125aSTAT3

Identifiers

PMID26389681
PMCPMC4694830
OpenAlexW1531496913

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.