Long noncoding RNA XIST participates in bladder cancer by downregulating p53 via binding to TET1

Bo Hu1, Guowei Shi1, Qian Li2

  • 1Department of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.

Insights

Long noncoding RNA XIST (XIST) knockdown suppresses bladder cancer cell migration and proliferation. XIST downregulates p53 by binding to TET1, revealing a novel XIST-TET1-p53 regulatory network in bladder cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in cellular regulatory networks and disease pathology.
  • The lncRNA X-inactive specific transcript (XIST) is known to influence cell migration, proliferation, and apoptosis in various cancers.

Purpose of the Study:

  • To investigate the role of XIST in bladder cancer.
  • To determine the effects of XIST on bladder cancer cell proliferation, migration, and apoptosis.
  • To elucidate the molecular mechanism underlying XIST's function in bladder cancer.

Main Methods:

  • Cell proliferation, cell cycle, and apoptosis assays were performed on bladder cancer cells.
  • Cell migration was assessed using cell migration assays.
  • RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays were used to examine the XIST-TET1 interaction and TET1's regulation of p53.
  • Western blot analysis was conducted to detect p53 expression levels following XIST manipulation.

Main Results:

  • Knockdown of XIST significantly inhibited cell migration and proliferation in vitro.
  • The study confirmed that XIST binds to TET1.
  • XIST was found to downregulate p53 expression through its interaction with TET1.

Conclusions:

  • lncRNA XIST plays a role in bladder cancer progression.
  • The XIST-TET1-p53 axis represents a potential regulatory network in bladder cancer.
  • Targeting XIST may offer a therapeutic strategy for bladder cancer.

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