Evidence map›Paper›PMID 36335987›Full record

ArticleJournal of gynecologic oncology2022

LncRNA XIST promotes carboplatin resistance of ovarian cancer through activating autophagy via targeting miR-506-3p/FOXP1 axis.

Xiaoyan Xia, Zikui Li, Yaojun Li, Feng Ye, Xiaoming Zhou

Open access · diamondAbstract read
In one paragraph

Article in Journal of gynecologic oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  15. Role of autophagy and its regulation by noncoding RNAs in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  16. Review
  17. lncHUB2: aggregated and inferred knowledge about human and mouse lncRNAs.Database : the journal of biological databases and curation · 2023
    Article
  18. Review
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  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

5 authors at 2 institutions in 1 country.

Xiaoyan XiaScientific Research Department, Changsha Health Vocational College, Changsha, P.R. China.ORCID 0000-0002-7661-5445
Zikui LiDepartment of Obstetrics and Gynecology, The Fist Hospital of Hunan University of Chinese Medicine, Changsha, P.R. China.ORCID 0000-0002-0334-834X
Yaojun LiNursing College of Changsha Health Vocational College, Changsha, P.R. China.ORCID 0000-0002-6196-6218
Feng YeNursing College of Changsha Health Vocational College, Changsha, P.R. China.ORCID 0000-0002-1947-9467
Xiaoming ZhouDepartment of Cardiology, The Fist Hospital of Hunan University of Chinese Medicine, Changsha, P.R. China. 43960905@qq.com.ORCID 0000-0003-1189-6677
Changsha University · CNHunan University of Traditional Chinese Medicine · CN

Funding

Natural Sciences Funding Project of Hunan Provinc 2020JJ7097
6 · The paper itself

Abstract

objectiveResistance to chemotherapy drugs makes ovarian cancer (OC) difficult to treat and ultimately kills patients. Long non-coding RNAs are closely related to carboplatin resistance in OC. In present study, we explored the role of lncRNA X-inactive specific transcript (XIST) on carboplatin resistance in OC.

methodsCell viability, proliferation, and apoptosis were assessed through 2,5-diphenyl-2H-tetrazolium bromide, colony formation, and flow cytometry assays, respectively. Microtubule-associated protein 1A/1B-light chain 3 expression was evaluated by immunofluorescence assay to analyze the cell autophagy. The interaction of XIST/miR-506-3p or miR-506-3p/forkhead box protein P1 (FOXP1) was analyzed using RNA immunoprecipitation (RIP) and dual-luciferases reporter assays. The function of XIST/miR-506-3p/FOXP1 axis in vivo was further confirmed by tumor xenograft study and immunohistochemistry.

resultsThe expression of XIST and FOXP1 increased while miR-506-3p decreased in OC and carboplatin resistance cells. XIST silencing repressed the proliferative and autophagic capacities of carboplatin resistance cells while promoted the apoptosis. XIST overexpression led to the opposite results. XIST targeted miR-506-3p and downregulated its expression. MiR-506-3p inhibition facilitated the proliferative and autophagic capacities while suppressed the apoptosis of cells, XIST knockdown reversed these effects. MiR-506-3p bound to FOXP1. XIST knockdown or miR-506-3p overexpression reversed the increase of cell proliferative and autophagic abilities and the decrease of apoptosis rate induced by FOXP1 overexpression. XIST affected autophagy and carboplatin resistance in vivo via regulating the miR-506-3p/FOXP1 axis.

conclusionXIST knockdown inhibited autophagy and carboplatin resistance of OC through FOXP1/protein kinase B (AKT)/mammalian target of rapamycin pathway by targeting miR-506-3p.

Indexed as

MicroRNAsOvarian NeoplasmsRNA, Long NoncodingApoptosisAutophagyCarboplatinCarcinoma, Ovarian EpithelialCell ProliferationFemaleForkhead Transcription FactorsHumansRepressor ProteinsCarboplatinForkhead Transcription FactorsFOXP1 protein, humanMicroRNAsMIRN506 microRNA, humanRepressor ProteinsRNA, Long NoncodingCarboplatinOvarian Cancer

Identifiers

PMID36335987
PMCPMC9634093
OpenAlexW4308688339

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.