Evidence map›Paper›PMID 31221168›Full record

ArticleMolecular cancer2019

A novel AR translational regulator lncRNA LBCS inhibits castration resistance of prostate cancer.

Peng Gu, Xu Chen, Ruihui Xie, Weibin Xie, Li Huang, Wen Dong, Jinli Han, Xiaodong Liu, Jihong Shen, Jian Huang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 150 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Peng GuDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Xu ChenDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. chenx457@mail.sysu.edu.cn.
Ruihui XieDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Weibin XieDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Li HuangDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Wen DongDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Jinli HanDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.
Xiaodong LiuDepartment of Urology, The 1st Affiliated Hospital of Kunming Medical University, Kunming, 650032, China.
Jihong ShenDepartment of Urology, The 1st Affiliated Hospital of Kunming Medical University, Kunming, 650032, China.
Jian HuangDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. huangj8@mail.sysu.edu.cn.
Tianxin LinDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. lintx@mail.sysu.edu.cn.ORCID 0000-0003-3180-8697
Sun Yat-sen University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgression to a castration resistance state is the main cause of deaths in prostate cancer (PCa) patients. Androgen Receptor (AR) signaling plays the central role in progression of Castration Resistant Prostate Cancer (CRPC), therefore understanding the mechanisms of AR activation in the milieu of low androgen is critical to discover novel approach to treat CRPC.

methodsFirstly, we explore the CRPC associated lncRNAs by transcriptome microarray. The expression and clinical features of lnc-LBCS are analyzed in three independent large-scale cohorts. The functional role and mechanism of lnc-LBCS are further investigated by gain and loss of function assays in vitro.

resultsThe expression of Lnc-LBCS was lower in CRPC cells lines and tissues. LBCS downregulation was correlated with higher Gleason Score, T stage and poor prognosis of PCa patients. LBCS overexpression decreases, whereas LBCS knockdown increases, the traits of castration resistance in prostate cancer cells under androgen ablated or AR blocked condition. Moreover, knockdown of LBCS was sufficient to activate AR signaling in the absence of androgen by elevating the translation of AR protein. Mechanistically, LBCS interacted directly with hnRNPK to suppress AR translation efficiency by forming complex with hnRNPK and AR mRNA.

conclusionsLnc-LBCS functions as a novel AR translational regulator that suppresses castration resistance of prostate cancer by interacting with hnRNPK. This sheds a new insight into the regulation of CRPC by lncRNA mediated AR activation and LBCS-hnRNPK-AR axis provides a promising approach to the treatment of CRPC.

Indexed as

5' Untranslated RegionsCell Line, TumorGene Expression ProfilingGene Expression Regulation, NeoplasticHeterogeneous-Nuclear Ribonucleoprotein KHumansMaleMicroRNAsNeoplasm StagingOligonucleotide Array Sequence AnalysisPrognosisProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSurvival Analysis5' Untranslated RegionsAR protein, humanHeterogeneous-Nuclear Ribonucleoprotein KHNRNPK protein, humanMicroRNAsReceptors, AndrogenAndrogen receptor (AR)Castration resistanceCastration resistance prostate Cancer (CRPC)hnRNPKlncRNA LBCS

Identifiers

PMID31221168
PMCPMC6585145
OpenAlexW2952810289

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.