SNHG7 interacts with PCBP2 to promote CDKN2A expression and modulate cuproptosis in colorectal cancer

Qiusan Chen1, Qiuyu Song1, Haonan Zhang1

  • 1Department of Gastroenterology; Guangdong Provincial Key Laboratory of Major Obstetric Diseases; Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology; The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Translational Oncology
|March 24, 2026
PubMed

Insights

Small nucleolar RNA host gene 7 (SNHG7) promotes colorectal cancer (CRC) by enhancing Cyclin dependent kinase inhibitor 2A (CDKN2A) expression via Poly(rC)-binding protein 2 (PCBP2) interaction. This study highlights SNHG7 as a potential therapeutic target for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) is a leading global malignancy.
  • Cuproptosis is a novel cell death pathway involving the CDKN2A gene.
  • SNHG7 and PCBP2 are implicated in tumorigenesis, but their role in CRC via cuproptosis is unclear.

Purpose of the Study:

  • To investigate the clinical role of cuproptosis-related SNHG7 in colorectal cancer.
  • To elucidate the molecular mechanism by which SNHG7 influences CRC progression.

Main Methods:

  • Cell culture and in vivo tumor formation in nude mice.
  • Quantitative PCR (qPCR) and Western blotting for gene and protein expression analysis.
  • RNA immunoprecipitation (RIP), lactate production assays, gel electrophoresis, and immunohistochemistry.

Main Results:

  • SNHG7 was found to interact with PCBP2.
  • This interaction enhances the expression of CDKN2A.
  • The SNHG7-PCBP2-CDKN2A axis modulates cuproptosis and promotes tumor glycolysis.

Conclusions:

  • SNHG7 promotes colorectal cancer progression by regulating cuproptosis and glycolysis.
  • SNHG7, in conjunction with PCBP2 and CDKN2A, represents a potential therapeutic target for CRC treatment.

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