CERS6 antisense RNA 1 promotes colon cancer via upregulating mitochondrial calcium uniporter

Juan Yu1, Xiaoguang Chen1, Jing Li1

  • 1Endoscopic Diagnosis and Treatment Center, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.

Abstract

Insights

Long non-coding RNA CERS6 antisense RNA 1 (CERS6-AS1) promotes colon cancer (CC) development by upregulating mitochondrial calcium uniporter. This study clarifies the role of CERS6-AS1 in CC progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Colon cancer (CC) is a prevalent digestive system malignancy.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
  • The specific function of lncRNA CERS6 antisense RNA 1 (CERS6-AS1) in CC pathogenesis was previously undefined.

Purpose of the Study:

  • To investigate the expression and functional role of CERS6-AS1 in colon cancer.
  • To elucidate the molecular mechanism by which CERS6-AS1 influences CC progression.

Main Methods:

  • Assessed CERS6-AS1 expression using The Cancer Genome Atlas and quantitative real-time polymerase chain reaction.
  • Evaluated CC cell function and tumor growth via in vitro and in vivo assays.
  • Utilized RNA pull down, RNA-binding protein immunoprecipitation, and luciferase reporter assays to determine molecular interactions.

Main Results:

  • CERS6-AS1 was significantly upregulated in colon adenocarcinoma tissues and cell lines.
  • CERS6-AS1 knockdown suppressed CC cell malignancy and tumor growth.
  • CERS6-AS1 acts as a competing endogenous RNA for microRNA-16-5p, targeting mitochondrial calcium uniporter (MCU) and enhancing MCU mRNA stability via the RNA-binding protein embryonic lethal abnormal vision like 1.

Conclusions:

  • CERS6-AS1 promotes colon cancer development.
  • The mechanism involves the upregulation of mitochondrial calcium uniporter expression.
  • CERS6-AS1 represents a potential therapeutic target for colon cancer.

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