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CDK5RAP2 is a Wnt target gene and promotes stemness and progression of oral squamous cell carcinoma

Yuehong Shen1,2, Yuling Chen1, Yuntao Lin1

  • 1Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital; Guangdong Provincial High-level Clinical Key Specialty; Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment; The Institute of Stomatology, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Guangdong, China.

Cell Death & Disease
|February 11, 2023
PubMed

Insights

CDK5RAP2 protein is highly expressed in oral squamous cell carcinoma (OSCC), promoting tumor growth and metastasis. Targeting CDK5RAP2 may offer a new strategy for treating OSCC by affecting cancer stem cells.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Oral squamous cell carcinoma (OSCC) is an aggressive cancer with poor prognosis.
  • The role of the microtubule regulatory protein CDK5RAP2 in OSCC remains unclear.

Purpose of the Study:

  • To investigate the expression, regulation, and function of CDK5RAP2 in OSCC.
  • To determine if CDK5RAP2 plays a role in OSCC tumorigenesis and cancer stem cell (CSC) characteristics.

Main Methods:

  • Analysis of CDK5RAP2 expression in OSCC tissues.
  • Investigation of CDK5RAP2 regulation by the Wnt signaling pathway.
  • Depletion of CDK5RAP2 in OSCC cells and assessment of its effects on cell behavior and mitosis.

Main Results:

  • CDK5RAP2 is highly expressed in OSCC, correlating with advanced clinical stage and lymph node metastasis.
  • CDK5RAP2 expression is regulated by the Wnt signaling pathway.
  • CDK5RAP2 depletion inhibits OSCC cell tumorigenesis, migration, and alters the cancer stem cell signature, disrupting spindle orientation during mitosis.

Conclusions:

  • CDK5RAP2 is a potential cancer stem cell marker in OSCC.
  • CDK5RAP2 plays a critical role in regulating the cancer stem cell population in OSCC through mechanisms involving mitosis and Wnt signaling.

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