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Selenium-binding protein 1 suppresses cell cycle progression via cyclin-dependent kinase 2 breakdown in colon

Xiaotian Zhang1, Dong Zhang1, Qichang Liu1

  • 1Department of General Surgery, Shanghai Fifth People's Hospital, Fudan University, Shanghai 200240, PR China.

Cellular Signalling
|December 6, 2025
PubMed

Insights

Selenium-binding protein 1 (SELENBP1) acts as a tumor suppressor in colorectal cancer by binding to cyclin-dependent kinase 2 (CDK2). SELENBP1 inhibits cancer cell growth by triggering CDK2 degradation, blocking cell cycle progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Selenium-binding protein 1 (SELENBP1) is a potential tumor suppressor in colorectal cancer (CRC).
  • The role of SELENBP1 in regulating cell cycle progression, specifically involving cyclin-dependent kinase 2 (CDK2), is not fully understood.

Purpose of the Study:

  • To investigate the interaction between SELENBP1 and CDK2 in CRC cells.
  • To determine how SELENBP1 influences the retinoblastoma protein (RB) signaling pathway and CDK2-mediated cell cycle progression.
  • To elucidate the molecular mechanism by which SELENBP1 inhibits CDK2 expression and function.

Main Methods:

  • Validation of intracellular binding between SELENBP1 and CDK2 using cultured CRC cells.
  • Assessment of SELENBP1's regulatory effects on RB signaling pathway activation.
  • Investigation of CDK2-mediated cell cycle progression.
  • Exploration of the mechanism underlying SELENBP1-induced inhibition of CDK2 expression, including ubiquitination studies.

Main Results:

  • Both ectopically induced and endogenously expressed SELENBP1 were found to bind to CDK2 in CRC cells.
  • SELENBP1 inhibited CDK2 expression and activated the RB signaling pathway.
  • Mechanistic studies indicated that SELENBP1 promotes CDK2 breakdown via ubiquitination, thereby suppressing cancer cell growth.

Conclusions:

  • SELENBP1 functions as a tumor suppressor in colorectal cancer.
  • SELENBP1 inhibits cell cycle progression and tumor growth by inducing ubiquitination-mediated degradation of CDK2.
  • SELENBP1's mechanism involves blocking the interphase and mitosis continuum, highlighting its potential as a therapeutic target.
Keywords:
Cell cycleColorectal cancerCyclin-dependent kinase 2Selenium-binding proteinUbiquitination

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