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Long noncoding RNA LINC00052 suppressed the proliferation, migration and invasion of glioma cells by upregulating

C-F Xu1, P Liu, J Tan

  • 1Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, China.hf0213@sina.com.

European Review for Medical and Pharmacological Sciences
|June 19, 2019
PubMed
Abstract

Insights

Long noncoding RNA LINC00052 is downregulated in glioma. Overexpression of LINC00052 inhibits glioma cell proliferation, migration, and invasion by upregulating kruppel-like factor 6 (KLF6).

Area of Science:

  • Molecular oncology
  • Noncoding RNA research
  • Cancer genomics

Background:

  • Long noncoding RNAs (lncRNAs) are increasingly implicated in carcinogenesis.
  • Dysregulation of specific lncRNAs is linked to various cancers, including glioma.
  • Understanding the role of lncRNAs like LINC00052 is crucial for glioma research.

Purpose of the Study:

  • To investigate the molecular mechanisms of lncRNA LINC00052 in glioma tumorigenesis.
  • To determine the functional role of LINC00052 in glioma cell behavior.
  • To explore the interaction between LINC00052 and kruppel-like factor 6 (KLF6) in glioma progression.

Main Methods:

  • Quantitative Real-time polymerase chain reaction (qRT-PCR) to assess LINC00052 expression in glioma tissues and cell lines.
  • In vitro assays (proliferation, transwell, wound healing) to evaluate LINC00052's effect on glioma cell behaviors.
  • qRT-PCR and Western blot to analyze the interaction between LINC00052 and KLF6.

Main Results:

  • LINC00052 expression was significantly downregulated in glioma samples compared to adjacent normal tissues.
  • Overexpression of LINC00052 suppressed glioma cell proliferation, invasion, and migration in vitro.
  • LINC00052 overexpression led to increased mRNA and protein levels of KLF6, with a positive correlation observed between LINC00052 and KLF6 expression in tumors.

Conclusions:

  • LINC00052 acts as a tumor suppressor in glioma by inhibiting cell migration, invasion, and proliferation.
  • The tumor-suppressive function of LINC00052 is mediated through the upregulation of KLF6.
  • LINC00052-KLF6 pathway represents a potential therapeutic target for glioma treatment.

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