Decrease of miR-622 expression suppresses migration and invasion by targeting regulation of DYRK2 in colorectal

Yong Wang1, Jie Sun2, Xilin Wei3

  • 1The 4th Department of Orthopedic Surgery, Central Hospital affiliated to Shenyang Medical College, Shenyang.

Abstract

Insights

Decreasing microRNA-622 (miR-622) levels suppresses colorectal cancer (CRC) cell migration and invasion by targeting Dual Specificity Tyrosine Phosphorylation-Regulated Kinase 2 (DYRK2). The miR-622/DYRK2 pathway presents a potential therapeutic target for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are implicated in tumor development, but the role of microRNA-622 (miR-622) in colorectal cancer (CRC) is debated.
  • Dual Specificity Tyrosine Phosphorylation-Regulated Kinase 2 (DYRK2) acts as a tumor suppressor, yet its regulatory mechanisms in CRC are not fully understood.

Purpose of the Study:

  • To investigate the role of miR-622 in colorectal cancer (CRC).
  • To elucidate the regulatory relationship between miR-622 and DYRK2 in CRC.
  • To assess the potential of the miR-622/DYRK2 axis as a therapeutic target for CRC.

Main Methods:

  • Quantitative real-time PCR, Western blot, and immunohistochemistry were used to assess miR-622 and DYRK2 expression.
  • Transwell assays evaluated the impact of miR-622 on CRC cell migration and invasion.
  • Dual-luciferase reporter assays and antisense experiments confirmed the direct interaction between miR-622 and DYRK2.

Main Results:

  • miR-622 expression was significantly upregulated in CRC tissues and cell lines, inversely correlating with DYRK2 expression.
  • Downregulation of miR-622 inhibited migration and invasion of CRC cells (SW1116 and SW480).
  • DYRK2 was confirmed as a direct target of miR-622, with miR-622 negatively regulating DYRK2 expression.

Conclusions:

  • Reduced miR-622 expression suppresses colorectal cancer cell migration and invasion through the targeted regulation of DYRK2.
  • The miR-622/DYRK2 pathway represents a promising molecular target for CRC treatment.

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