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Development of Compendium for Esophageal Squamous Cell Carcinoma
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CPSF3 regulates alternative polyadenylation of CNIH2 to promote esophageal squamous cell carcinoma progression.

Ying Zhang1, Dongchen Liu2, Dan Guo3

  • 1Department of Radiotherapy, Cancer Hospital of Shantou University Medical College, No. 7 Raoping Road, Shantou, Guangdong, 515041, China; Department of Clinical Research Center, Cancer Hospital of Shantou University Medical College, No. 7 Raoping Road, Shantou, Guangdong, 515041, China.

Cancer Letters
|May 8, 2024
PubMed
Summary

Alternative polyadenylation (APA) factor CPSF3 promotes esophageal cancer (ESCC) by altering CNIH2 mRNA. This leads to reduced tumor suppression by miR-125a-5p, driving cancer progression.

Keywords:
Alternative polyadenylationCNIH2CPSF3ESCC

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Alternative polyadenylation (APA) is a key post-transcriptional regulator implicated in cancer.
  • The precise role of APA in esophageal squamous cell carcinoma (ESCC) tumorigenesis is not fully understood.

Purpose of the Study:

  • To investigate the role of APA in ESCC.
  • To identify APA-related 3'UTR alterations affecting patient prognosis.
  • To examine the function of CPSF3 in ESCC progression.

Main Methods:

  • Analysis of TCGA RNA-seq data for APA events.
  • Immunohistochemistry and qRT-PCR to assess CPSF3 expression.
  • In vitro (cell proliferation, migration) and in vivo (animal models) experiments.
  • Iso-Seq and RNA-seq to analyze CNIH2 isoforms.
  • MiRNA binding site analysis.

Main Results:

  • Identified 3'UTR alterations in ESCC linked to prognosis and loss of tumor-suppressive miRNA sites.
  • Found high CPSF3 expression in ESCC tissues, correlating with poor prognosis.
  • CPSF3 overexpression enhanced ESCC cell proliferation and migration; knockdown inhibited these processes.
  • CPSF3 knockdown led to distal polyadenylation of CNIH2 mRNA, creating a long 3'UTR isoform.
  • The long CNIH2 isoform is targeted by miR-125a-5p, reducing CNIH2 protein levels.
  • CPSF3-driven ESCC tumorigenicity was mediated by CNIH2.

Conclusions:

  • CPSF3 promotes ESCC progression by upregulating CNIH2.
  • This occurs through APA-mediated loss of miR-125a-5p repression of CNIH2.
  • Targeting CPSF3 or modulating CNIH2/miR-125a-5p interactions may offer therapeutic strategies for ESCC.