Evidence map›Paper›PMID 32516753›Full record

ArticleAging2020

Highly expressed STAT1 contributes to the suppression of stemness properties in human paclitaxel-resistant ovarian cancer cells.

Fanchen Wang, Lingyun Zhang, Jiao Liu, Jinguo Zhang, Guoxiong Xu

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. S1PR1 suppresses lung adenocarcinoma progression through p-STAT1/miR-30c-5 p/FOXA1 pathway.Journal of experimental & clinical cancer research : CR · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. RBM15‑mediating MDR1 mRNA mInternational journal of oncology · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. 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.

Fanchen WangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Lingyun ZhangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Jiao LiuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Jinguo ZhangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Guoxiong XuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Jinshan Hospital of Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription-1 (STAT1) is an important factor in various cellular processes. The cancer stem cell (CSC) is considered as a tumor-initiating cell that drives the inner hierarchy in many cancers including epithelial ovarian cancer (EOC). Here, we explored for the first time the regulation of STAT1 on stemness properties in chemoresistant EOC cells. The paclitaxel (PTX)-resistant EOC cell line (OV3R-PTX) was derived from PTX-sensitive OVCAR-3 cells treated by the PTX regimen. A single cell clone OV3R-PTX-B4 was selected by fluorescence-activated cell sorting. PTX-resistant cells grew slowly in conventional 2D and 3D cultures, but tumor xenograft with PTX-resistant cells grew fast in nude mice. Interestingly, OV3R-PTX-B4 cells shared the characteristics of CSCs and stemness properties were found to be increased in the non-adherent spheroid culture system. The PTX-resistant cells had a high expression of CSC-related markers and low expression of STAT1 that had a high methylation level of CpG in its promoter region. Overexpressed STAT1 suppressed stemness properties, cell proliferation, and colony formation and favored the overall survival of patients with EOC. In summary, these data indicate a regulatory mechanism of STAT1 underlying drug resistance and provide a potential therapeutic application for EOC patients with PTX resistance.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisCell Line, TumorCell ProliferationCell SurvivalDrug Resistance, NeoplasmFemaleHumansMiceMice, NudeNeoplasm TransplantationNeoplastic Stem CellsOvarian NeoplasmsPaclitaxelSignal TransductionAntineoplastic Agents, PhytogenicPaclitaxelSTAT1 protein, humanSTAT1 Transcription Factorchemoresistancemethylationovarian cancerSTAT1stem cell

Identifiers

PMID32516753
PMCPMC7346083
OpenAlexW3032908602

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.