Evidence map›Paper›PMID 28235236›Full record

ArticleCancer science2017

PVT1-derived miR-1207-5p promotes breast cancer cell growth by targeting STAT6.

Chen Yan, Yaqing Chen, Weiwei Kong, Liya Fu, Yunde Liu, Qingjuan Yao, Yuhua Yuan

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

52 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Protein and peptide letters · 2024
    Article
  9. Review
  10. Review
  11. Mechanisms of Long Non-Coding RNA in Breast Cancer.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022
    Review
  17. Long non-coding RNA PVT1 facilitates cell migration and invasion by regulating miR-148a-3p and ROCK1 in breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  18. Review
  19. Article
  20. Article
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

7 authors at 4 institutions in 1 country.

Chen YanSchool of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yaqing ChenSchool of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Weiwei KongBlood Transfusion Branch, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Liya FuDepartment of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China.
Yunde LiuSchools of Laboratory Medicine, Tianjin Medical University, Tianjin, China.
Qingjuan YaoGeneral Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Yuhua YuanClinical Laboratory Diagnostics, Tianjin Medical University General Hospital, Tianjin, China.
Tianjin Medical University · CNTianjin Medical University General Hospital · CNNankai University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence indicates that ectopic expression of non-coding RNAs are responsible for breast cancer progression. Increased non-coding RNA PVT1, the host gene of microRNA-1207-5p (miR-1207-5p), has been associated with breast cancer proliferation. However, how PVT1 functions in breast cancer is still not clear. In this study, we show a PVT1-derived microRNA, miR-1207-5p, that promotes the proliferation of breast cancer cells by directly regulating STAT6. We first confirm the positive correlated expression pattern between PVT1 and miR-1207-5p by observing consistent induced expression by estrogen, and overexpression in breast cancer cell lines and breast cancer patient specimens. Moreover, silence of PVT1 also decreased miR-1207-5p expression. Furthermore, increased miR-1207-5p expression promoted, while decreased miR-1207-5p expression suppressed, cell proliferation, colony formation, and cell cycle progression in breast cancer cell lines. Mechanistically, a novel target of miR-1207-5p, STAT6, was identified by a luciferase reporter assay. Overexpression of miR-1207-5p decreased the levels of STAT6, which activated CDKN1A and CDKN1B to regulate the cell cycle. We also confirmed the reverse correlation of miR-1207-5p and STAT6 expression levels in breast cancer samples. Therefore, our findings reveal that PVT1-derived miR-1207-5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression. These findings suggest miR-1207-5p might be a potential target for breast cancer therapy.

Indexed as

BreastBreast NeoplasmsCell CycleCell LineCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHEK293 CellsHumansMicroRNAsMiddle AgedRNA, Long NoncodingSTAT6 Transcription FactorMicroRNAsMIRN1207 microRNA, humanPVT1 long-non-coding RNA, humanRNA, Long NoncodingSTAT6 protein, humanSTAT6 Transcription FactorBreast cancercell proliferationmiR-1207-5pPVT1STAT6

Identifiers

PMID28235236
PMCPMC5448618
OpenAlexW2590250806

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.