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Long non-coding RNA DILC suppresses bladder cancer cells progression.

Qian-Yun Ma1, Shu-Ying Li2, Xi-Zhou Li3

  • 1Department of Urology surgery, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China.

Gene
|June 10, 2019
PubMed
Summary

Long non-coding RNA DILC (lnc-DILC) acts as a tumor suppressor in bladder cancer (BC). Overexpression of lnc-DILC inhibits BC cell proliferation and metastasis by inactivating the STAT3 pathway.

Keywords:
Bladder cancerProliferationSTAT3Self-renewallnc-DILC

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play crucial roles in various cancers, including bladder cancer (BC).
  • Previous research identified lnc-DILC as a tumor suppressor in liver and colorectal cancers.
  • The specific function of lnc-DILC in BC progression was previously unknown.

Purpose of the Study:

  • To investigate the role of lnc-DILC in bladder cancer.
  • To determine the underlying molecular mechanism of lnc-DILC's function in BC.

Main Methods:

  • Analysis of lnc-DILC expression in human bladder cancer tissues.
  • Overexpression of lnc-DILC in BC cells to assess effects on proliferation, metastasis, and cancer stem cells (CSCs).
  • Utilizing a STAT3 inhibitor (S3I-201) to confirm the involvement of the STAT3 pathway.

Main Results:

  • lnc-DILC was found to be downregulated in human bladder cancer tissues.
  • Overexpression of lnc-DILC significantly suppressed BC cell proliferation, metastasis, and CSC expansion.
  • Inhibition of the STAT3 pathway by lnc-DILC was confirmed using a specific STAT3 inhibitor, which reversed the suppressive effects.

Conclusions:

  • lnc-DILC functions as a novel tumor suppressor in bladder cancer.
  • lnc-DILC inhibits BC progression and metastasis by inactivating the STAT3 signaling pathway.