LNC-LBCS

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Lnc-LBCS,as a regulator, plays an important tumor-suppressor role in BCSCs' self-renewal and suppresses castration resistance of prostate cancer by interacting with hnRNPK. [1][2]

Annotated Information

Name

Approved symbol:LNC-LBCS

Approved name:lncRNA bladder and prostate cancer suppressor, hnRNPK interacting

HGNC ID HGNC:54418

Alias symbol:LBCS

RefSeq ID:NR_134649

Characteristics

Please input information here.

Function

Lnc-LBCS markedly inhibits self-renewal, chemoresistance, and tumor initiation of BCSCs both in vitro and in vivo.[1]. LBCS interacted directly with hnRNPK to suppress AR translation efficiency by forming complex with hnRNPK and AR mRNA.[2]

Regulation

Lnc-LBCS directly binds to heterogeneous nuclear ribonucleoprotein K (hnRNPK) and enhancer of zeste homolog 2 (EZH2), and serves as a scaffold to induce the formation of this complex to repress SRY-box 2 (SOX2) transcription via mediating histone H3 lysine 27 tri-methylation. [1] Knockdown of LBCS was sufficient to activate AR signaling in the absence of androgen by elevating the translation of AR protein. [2]

Expression

Lnc-LBCS is significantly downregulated in BCSCs and cancer tissues, and correlates with tumor grade, chemotherapy response, and prognosis.[1] The expression of Lnc-LBCS was lower in CRPC cells lines and tissues.[2]

Diseases

Bladder cancer[1] Castration Resistant Prostate Cancer (CRPC)[2]

Labs working on this lncRNA

  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.[1]
  • Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.[1]
  • Department of Pediatric Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.[1]
  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. lintx@mail.sysu.edu.cn urolhj@sina.com.[1]
  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China.[2]
  • Department of Urology, The 1st Affiliated Hospital of Kunming Medical University, Kunming, 650032, China.[2]
  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. chenx457@mail.sysu.edu.cn.[2]
  • Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China. chenx457@mail.sysu.edu.cn.[2]
  • Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.[2]
  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. huangj8@mail.sysu.edu.cn.[2]
  • Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107. W. Yanjiang Road, Guangzhou, 510120, China. lintx@mail.sysu.edu.cn.[2]
  • Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China. lintx@mail.sysu.edu.cn.[2]
  • RNA Biomedical Institute, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China. lintx@mail.sysu.edu.cn.[2]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Chen X, Xie R, Gu P, Huang M, Han J, Dong W, Xie W, Wang B, He W, Zhong G, Chen Z, Huang J, Lin T. Long Noncoding RNA LBCS Inhibits Self-Renewal and Chemoresistance of Bladder Cancer Stem Cells through Epigenetic Silencing of SOX2. Clin Cancer Res. 2019 Feb 15;25(4):1389-1403. doi: 10.1158/1078-0432.CCR-18-1656.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 Gu P, Chen X, Xie R, Xie W, Huang L, Dong W, Han J, Liu X, Shen J, Huang J, Lin T. A novel AR translational regulator lncRNA LBCS inhibits castration resistance of prostate cancer. Mol Cancer. 2019 Jun 20;18(1):109. doi: 10.1186/s12943-019-1037-8.