Targeting LncRNA EPIC1 to inhibit human colon cancer cell progression

Qiong Wu1, Jue Wei1, Chen Zhao1

  • 1Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Aging
|November 10, 2020
PubMed

Insights

Long non-coding RNA EPIC1 (Lnc-EPIC1) promotes human colon cancer progression by binding to MYC. Silencing Lnc-EPIC1 inhibits cancer cell growth, migration, and invasion, while its overexpression enhances these processes.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play crucial roles in cellular processes.
  • MYC protein is a key regulator of cell growth and proliferation, and its dysregulation is common in cancer.
  • The specific role of Lnc-EPIC1 in colon cancer has not been fully elucidated.

Purpose of the Study:

  • To investigate the expression levels of Lnc-EPIC1 in human colon cancer.
  • To determine the functional role of Lnc-EPIC1 in colon cancer cell proliferation, migration, invasion, and apoptosis.
  • To elucidate the interaction between Lnc-EPIC1 and MYC in colon cancer cells.

Main Methods:

  • Quantitative real-time PCR to assess Lnc-EPIC1 expression in colon cancer tissues and cells.
  • siRNA-mediated knockdown and ectopic overexpression of Lnc-EPIC1 in colon cancer cell lines.
  • Cell proliferation, migration, invasion, and apoptosis assays.
  • RNA-immunoprecipitation and RNA pull-down assays to confirm direct binding of Lnc-EPIC1 to MYC.
  • Western blotting to analyze the expression of MYC target genes.

Main Results:

  • Lnc-EPIC1 expression was significantly elevated in human colon cancer tissues and cells compared to normal tissues and cells.
  • Lnc-EPIC1 silencing inhibited colon cancer cell growth, proliferation, migration, and invasion, and induced apoptosis.
  • Lnc-EPIC1 overexpression promoted colon cancer cell growth, proliferation, migration, and invasion.
  • Lnc-EPIC1 directly binds to MYC protein in colon cancer cells.
  • Silencing or overexpression of Lnc-EPIC1 altered the expression of MYC target proteins (cyclin A, cyclin D, CDK9) in a manner consistent with MYC regulation.
  • Functional alterations of Lnc-EPIC1 were dependent on MYC expression, as Lnc-EPIC1 manipulation had no effect in MYC-knockout cells.

Conclusions:

  • Overexpressed Lnc-EPIC1 is a critical driver of human colon cancer progression.
  • Lnc-EPIC1 exerts its oncogenic functions by directly interacting with MYC, influencing MYC target gene expression and downstream cellular processes.
  • Lnc-EPIC1 represents a potential therapeutic target for colon cancer treatment.

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