Evidence map›Paper›PMID 31776419›Full record

ArticleScientific reports2019

Sema4C mediates EMT inducing chemotherapeutic resistance of miR-31-3p in cervical cancer cells.

Li Jing, Wang Bo, Feng Yourong, Wang Tian, Wang Shixuan, Wu Mingfu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  9. Oncology letters · 2022
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  12. SEMAPHORINS and their receptors: focus on the crosstalk between melanoma and hypoxia.Journal of experimental & clinical cancer research : CR · 2021
    Review
  13. Review
  14. MiRNA-mediated EMT and CSCs in cancer chemoresistance.Experimental hematology & oncology · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
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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

6 authors at 2 institutions in 1 country.

Li JingDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China.
Wang BoDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China.
Feng YourongDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China.
Wang TianDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China.
Wang ShixuanDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China. sxwang@tjh.tjmu.edu.cn.
Wu MingfuDepartment Gynecology, Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China. mingfuwutj@163.com.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sema4C, the target of many miRNAs, is involved in EMT-mediated chemotherapeutic resistance of many malignant tumors. However, the underlying upstream regulatory mechanisms of Sema4C-induced EMT and Sema4C-mediated drug resistance are still unclear. The aim of this study was to explore the potential role of miR-31-3p/Sema4C in regulating EMT in cisplatin-resistant (CR) cervical cancer cells. High expression levels of Sema4C were more frequently found in cervical cancer tissues and were associated with poor prognosis, whereas miR-31-3p was significantly downregulated in cervical cancer tissues, which was associated with shorter disease-free and overall survival. Overexpression of miR-31-3p inhibited malignant behaviors and EMT of cervical cancer cells in vitro. Furthermore, miR-31-3p was identified to directly target Sema4C, and upregulation of miR-31-3p reversed EMT-mediated biological functions, including cisplatin resistance of Sema4C in cervical cancer cells. These results suggest that Sema4C promoted EMT-mediated cisplatin resistance in cervical cancer cells and that this effect was inhibited by overexpression of miR-31-3p. Thus, silencing Sema4C or overexpression of miR-31-3p could be a novel approach to treat drug resistance to chemotherapy in cervical cancers.

Indexed as

Drug Resistance, NeoplasmEpithelial-Mesenchymal TransitionAdultAntineoplastic AgentsCisplatinDown-RegulationFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansMicroRNAsMiddle AgedSemaphorinsUterine Cervical NeoplasmsAntineoplastic AgentsCisplatinMicroRNAsMIRN31 microRNA, humanSema4c protein, humanSemaphorins

Identifiers

PMID31776419
PMCPMC6881343
OpenAlexW2991266834

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.