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FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1

Lei Yang1, Dawei Ge2, Xi Chen1

  • 1Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

Biochemical and Biophysical Research Communications
|June 3, 2018
PubMed

Insights

FOXP4-AS1 is overexpressed in osteosarcoma (OS) and promotes tumor growth and metastasis. This long non-coding RNA is an independent risk factor for OS prognosis, impacting patient survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Osteosarcoma (OS) is a prevalent bone cancer in children and adolescents.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in various cancers.

Purpose of the Study:

  • To investigate the role of FOXP4-AS1 in osteosarcoma (OS) development.
  • To elucidate the underlying molecular mechanisms of FOXP4-AS1 in OS.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to detect FOXP4-AS1 expression in OS tissues.
  • In vitro cell experiments (MG63 and U2OS cells) to assess proliferation, migration, invasion, and cell cycle.
  • RNA immunoprecipitation (RIP) assay to determine interactions between FOXP4-AS1, LSD1, and EZH2.

Main Results:

  • FOXP4-AS1 was significantly overexpressed in OS tissues compared to adjacent tissues.
  • High FOXP4-AS1 expression correlated with poorer disease-free and overall survival, larger tumor size, and lung metastasis.
  • Overexpression of FOXP4-AS1 enhanced OS cell proliferation, migration, and invasion, while knockdown inhibited these processes.
  • FOXP4-AS1 was found to inhibit LATS1 expression by interacting with LSD1 and EZH2, thereby promoting OS progression.

Conclusions:

  • FOXP4-AS1 is upregulated in osteosarcoma and serves as an independent prognostic risk factor.
  • Increased FOXP4-AS1 expression promotes OS cell proliferation, migration, and cell cycle progression while inhibiting apoptosis.
  • FOXP4-AS1 contributes to OS development and progression by downregulating LATS1 through binding with LSD1 and EZH2.
Keywords:
EZH2FOXP4-AS1LATS1LSD1Osteosarcoma

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