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XIST sponges miR-320d to promote chordoma progression by regulating ARF6

Yonggang Wang1, Zhouzhou Tang2, Weichun Guo1

  • 1Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.

Journal of Bone Oncology
|July 28, 2022
PubMed
Abstract

Insights

Long non-coding RNA XIST promotes chordoma progression by enhancing cell proliferation, migration, invasion, and glycolysis. Silencing XIST inhibits tumor growth by regulating the microRNA-320d/ADP-ribosylation factor 6 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are implicated in various cancers, including chordoma.
  • The specific role of lncRNA X-inactive specific transcript (XIST) in chordoma remains to be fully elucidated.

Purpose of the Study:

  • To investigate the function and mechanism of lncRNA XIST in chordoma.
  • To explore the potential of XIST as a therapeutic target for chordoma.

Main Methods:

  • Quantitative real-time PCR and western blot for RNA and protein expression.
  • Cell proliferation, migration, invasion, and glycolysis assays (MTT, EdU, colony formation, Transwell, ECAR, lactate production).
  • Bioinformatics, dual-luciferase reporter, and RNA-pull down assays to confirm interactions; xenograft model for in vivo validation.

Main Results:

  • XIST was overexpressed in chordoma tissues and promoted chordoma cell proliferation, migration, invasion, and glycolysis.
  • XIST functioned as a molecular sponge for microRNA-320d (miR-320d), upregulating ADP-ribosylation factor 6 (ARF6) expression.
  • XIST knockdown inhibited tumor growth in vivo, while ARF6 overexpression reversed these inhibitory effects.

Conclusions:

  • XIST knockdown inhibits chordoma progression by regulating the miR-320d/ARF6 axis.
  • This study provides novel insights into chordoma pathogenesis and suggests XIST as a potential therapeutic target.
Keywords:
ARF6ChordomaXISTmiR-320d

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