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Long non-coding RNA LOC554202 modulates chordoma cell proliferation and invasion by recruiting EZH2 and regulating

Xianli Ma1, Shengjin Qi2, Zhenying Duan2

  • 1College of Pharmacy, Guilin Medical University, Guilin, Guangxi, China.

Cell Proliferation
|October 1, 2017
PubMed
Abstract

Insights

Long non-coding RNA LOC554202 promotes chordoma progression by upregulating EZH2 and RNF144B while downregulating miR-31. Targeting LOC554202 may offer a therapeutic strategy for chordoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Chordoma is a rare, malignant bone tumor originating from notochordal remnants.
  • Long non-coding RNA LOC554202, a host gene for miR-31, is implicated in various cancers, but its role in chordoma is largely unknown.

Purpose of the Study:

  • To elucidate the relationship between LOC554202, miR-31, and EZH2 in chordoma progression.
  • To investigate the functional role of LOC554202 in chordoma cell behavior and tumor growth.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot to assess expression levels of LOC554202, miR-31, EZH2, RNF144B, and EMT markers.
  • Cell proliferation, apoptosis, migration, and invasion assays in chordoma cell lines transfected with siRNA or miRNA mimics.
  • RNA pull down, RIP assay, and Luciferase Reporter Assay to confirm molecular interactions.
  • In vivo tumor xenograft models to evaluate the anti-tumour effects.

Main Results:

  • Elevated LOC554202 expression correlated with decreased miR-31 levels in chordoma tissues.
  • Knockdown of LOC554202 or overexpression of miR-31 inhibited chordoma cell proliferation, migration, and invasion.
  • LOC554202 directly upregulates EZH2, which in turn suppresses miR-31 expression.
  • miR-31 inhibition led to increased RNF144B expression and promoted metastasis.
  • In vivo studies confirmed that LOC554202 knockdown suppressed tumor growth by inhibiting the EZH2/miR-31 pathway and RNF144B activation.

Conclusions:

  • LOC554202 plays a significant role in chordoma progression.
  • The mechanism involves direct upregulation of EZH2 and indirect promotion of the oncogene RNF144B via miR-31.
  • Targeting LOC554202 presents a potential therapeutic avenue for chordoma.

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