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Long Non-coding RNA X-Inactive Specific Transcript Mediates Cell Proliferation and Intrusion by Modulating the

Qinhua Liu1, Ruonan Ran2, Zhengsheng Wu3

  • 1Department of Hematology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Frontiers in Cell and Developmental Biology
|December 28, 2020
PubMed

Insights

This study reveals that XIST long non-coding RNA promotes Extranodal natural killer/T-cell lymphoma (ENKL) growth by sponging miR-497, increasing Bcl-w. Inhibiting Bcl-w offers a therapeutic strategy for ENKL.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Extranodal natural killer/T-cell lymphoma (ENKL) is an aggressive non-Hodgkin lymphoma with limited therapeutic options.
  • Dysregulation of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) plays a crucial role in tumorigenesis.
  • Understanding lncRNA-miRNA-mRNA interactions is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of XIST (X-inactive specific transcript) in ENKL pathogenesis.
  • To elucidate the interaction between XIST, miR-497, and its downstream target Bcl-w in ENKL.
  • To explore the therapeutic potential of targeting the XIST/miR-497/Bcl-w axis in ENKL.

Main Methods:

  • Analysis of XIST expression in ENKL patients and cell lines (in vivo and in vitro).
  • lncRNA-miRNA interaction database screening to identify XIST targets, selecting miR-497.
  • Evaluation of XIST and miR-497 effects on downstream Bcl-w expression and ENKL cell proliferation/migration.
  • Assessment of Bcl-w inhibition using ABT737 to overcome XIST effects.

Main Results:

  • XIST expression was significantly upregulated in ENKL patient blood and cell lines.
  • XIST knockdown inhibited ENKL cell proliferation and migration.
  • A negative interaction between XIST and miR-497 was confirmed, with XIST acting as a sponge for miR-497.
  • XIST knockdown reduced Bcl-w protein levels, indicating Bcl-w is a downstream target of miR-497.
  • Inhibition of Bcl-w by ABT737 suppressed ENKL proliferation and migration by inducing apoptosis, overcoming XIST overexpression.

Conclusions:

  • XIST promotes ENKL cell proliferation and migration by sponging miR-497 and upregulating Bcl-w.
  • The XIST/miR-497/Bcl-w axis represents a novel therapeutic target for ENKL.
  • Targeting Bcl-w offers a potential strategy to overcome XIST-driven ENKL progression.
Keywords:
ENKLlncRNAmiRNAmigrationproliferation

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