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Functional Roles of DYRK2 as a Tumor Regulator

Yuta Mochimaru1, Kiyotsugu Yoshida1

  • 1Department of Biochemistry, The Jikei University School of Medicine, Tokyo 105-8461, Japan.

Current Issues in Molecular Biology
|October 27, 2023
PubMed

Insights

Dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) has a dual role in cancer, acting as both a tumor suppressor and oncogene. Further research, especially using genetically modified mice, is needed to clarify its complex functions in tumorigenesis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) is implicated in critical cellular processes including apoptosis, DNA repair, cell cycle regulation, and embryogenesis.
  • DYRK2's role in tumorigenesis is complex, with conflicting reports suggesting it can act as both a tumor suppressor and an oncogene across different cancer types.
  • Understanding the conserved functions of DYRK2 in cancer is challenging due to its reported dual role.

Purpose of the Study:

  • To review and synthesize the current understanding of DYRK2's functions across various human cancers.
  • To highlight the discrepancies in reported DYRK2 functions and identify knowledge gaps.
  • To emphasize the need for advanced research models to elucidate DYRK2's oncogenic or tumor-suppressive roles.

Main Methods:

  • Comprehensive literature review of studies investigating DYRK2 in cancer.
  • Analysis of findings from patient tissue samples.
  • Evaluation of evidence from cell line and xenograft studies.

Main Results:

  • DYRK2 exhibits context-dependent roles in tumorigenesis, functioning as both a tumor suppressor and an oncogene.
  • Current research using cell lines and xenografts provides limited insight into DYRK2's in vivo functions.
  • Significant variability exists in reported DYRK2 functions across different cancer types.

Conclusions:

  • The precise role of DYRK2 in cancer remains elusive due to its contradictory functions.
  • Further investigation using genetically modified mouse models is crucial for a deeper understanding of DYRK2's functional duality in cancer.
  • Clarifying DYRK2's mechanisms is essential for potential therapeutic strategies in oncology.
Keywords:
DYRK2non-solid tumorsolid tumor

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