Evidence map›Paper›PMID 32943985›Full record

ArticleCancer cell international2020

XIST lost induces ovarian cancer stem cells to acquire taxol resistance via a KMT2C-dependent way.

Ruili Huang, Lijuan Zhu, Yali Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Loss of XIST lncRNA unlocks stemness and cellular plasticity in ovarian cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Potential roles of lncRNA-XIST/miRNAs/mRNAs in human cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  10. Article
  11. Article
  12. Long noncoding RNAGenes & diseases · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021
    Review
  17. Review
  18. Review
  19. Review
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

3 authors at 1 institution in 1 country.

Ruili HuangDepartment of Gynaecology and Obstetrics, The First People's Hospital of Shangqiu, Henan, No. 292 Kaixuan South Road, 476100 Shangqiu, Henan People's Republic of China.ORCID 0000-0002-0222-2817
Lijuan ZhuDepartment of Gynaecology and Obstetrics, The First People's Hospital of Shangqiu, Henan, No. 292 Kaixuan South Road, 476100 Shangqiu, Henan People's Republic of China.
Yali ZhangDepartment of Gynaecology and Obstetrics, The First People's Hospital of Shangqiu, Henan, No. 292 Kaixuan South Road, 476100 Shangqiu, Henan People's Republic of China.
Shangqiu First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsThe expression levels of long non-coding RNA XIST are significantly associated with paclitaxel (Pac) sensitivity in ovarian cancer, but the mechanism of action remains unclear. Therefore, this experimental design was based on lncRNA XIST analysis to regulate the effect of XIST on the tumor stem cell and paclitaxel sensitivity in ovarian cancer.

methodsSphere assay and fluorescence activated cell sorting (FACS) were used to determine the expression levels of XIST and sensitivity to paclitaxel treatment. The effect of the proliferation was detected by MTT assay. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for lncRNA XIS and KMT2C. The expression of KMT2C was detected by RT-qPCR and Western blotting. RT-qPCR was used to detect the expression of cancer stem cell-associated genes SOX2, OCT4 and Nanog. The tumor changes in mice were detected by in vivo experiments in nude mice.

resultsThere was an inverse correlation between the expression of XIST and cancer stem cell (CD44 + /CD24-) population. XIST promoted methylation of histone H3 methylation at lysine 4 by enhancing the stability of lysine (K)-specific methyltransferase 2C (KMT2C) mRNA. XIST acted on the stability of KMT2C mRNA by directly targeting miR-93-5p. Overexpression of miR-93-5p can reverse the XIST overexpression-induced KMT2C decrease and sphere number increase. Overexpression of KMT2C inhibited XIST silencing-induced proliferation of cancer stem cells, and KMT2C was able to mediate paclitaxel resistance induced by XIST in ovarian cancer. The study found that XIST can affect the expression of KMT2C in the ovarian cancer via targeting miR-93-5p.

conclusionXIST promoted the sensitivity of ovarian cancer stem cells to paclitaxel in a KMT2C-dependent manner.

Indexed as

KMT2CLncRNA XISTOvarian cancerProliferationTumor stem cells

Identifiers

PMID32943985
PMCPMC7487955
OpenAlexW3083268554

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.