Evidence map›Paper›PMID 32089062›Full record

ArticleCancer biology & therapy2020

Knockdown of lncRNA CCAT1 enhances sensitivity of paclitaxel in prostate cancer via regulating miR-24-3p and FSCN1.

Xiaohui Li, Xingtao Han, Pengtao Wei, Jinhui Yang, Jiantao Sun

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  5. Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025
    Review
  6. Article
  7. LncRNAs in modulating cancer cell resistance to paclitaxel (PTX) therapy.Medical oncology (Northwood, London, England) · 2024
    Review
  8. Review
  9. Review
  10. Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024
    Review
  11. Review
  12. 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

5 authors at 1 institution in 1 country.

Xiaohui LiDepartment of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Xingtao HanDepartment of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Pengtao WeiDepartment of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Jinhui YangDepartment of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Jiantao SunDepartment of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance limits the efficacy of chemotherapy in human cancers. Previous studies reported that long noncoding RNA colon cancer-associated transcript 1 (CCAT1) regulated progression of prostate cancer (PCa). However, the potential role of CCAT1 in the sensitivity of paclitaxel (PTX) in PCa and its mechanism remain largely unknown. The PTX-resistant PCa cells were established in PC3 and DU145 cells by increasing concentrations of PTX. The expressions of CCAT1, microRNA-24-3p (miR-24-3p) and fascin1 (FSCN1) were measured by quantitative real-time polymerase chain reaction. The viability and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry and western blot, respectively. The interaction among CCAT1, miR-24-3p and FSCN1 was explored by luciferase activity, RNA immunoprecipitation, RNA pull-down and western blot, respectively. Results showed that the expressions of CCAT1 were up-regulated and miR-24-3p was down-regulated in PCa and PTX-resistant PCa cells (PC3-TXR and DU145-TXR). Knockdown of CCAT1 or overexpression of miR-24-3p inhibited survival rate, half maximal inhibitory concentration (IC50) of PTX but increased apoptosis in PC3-TXR and DU145-TXR cells after treatment of PTX. miR-24-3p was bound to CCAT1 and its abrogation reversed knockdown of CCAT1-mediated increase of PTX sensitivity in PC3-TXR and DU145-TXR cells. Moreover, FSCN1 restoration attenuated miR-24-3p-mediated inhibition of PTX resistance. Besides, FSCN1 level was enhanced in PCa and PTX-resistant PCa cells and regulated by CCAT1 and miR-24-3p. Our data suggested interference of CCAT1 contributed to PTX sensitivity in PCa by regulating miR-24-3p and FSCN1, indicating a novel avenue for treatment of PCa through regulating chemoresistance.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAntineoplastic Agents, PhytogenicApoptosisCarrier ProteinsCell Line, TumorHumansMaleMicrofilament ProteinsMicroRNAsPaclitaxelProstatic NeoplasmsRNA, Long NoncodingSignal TransductionUp-RegulationAntineoplastic Agents, PhytogenicCarrier ProteinsCCAT1 long noncoding RNA, humanFSCN1 protein, humanMicrofilament ProteinsMicroRNAsMIRN24 microRNA, humanPaclitaxelRNA, Long NoncodingCCAT1FSCN1miR-24-3ppaclitaxel sensitivityProstate cancer

Identifiers

PMID32089062
PMCPMC7515504
OpenAlexW3006823004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.