microRNA-622 upregulates cell cycle process by targeting FOLR2 to promote CRC proliferation

BMC Cancer. 2024 Jan 2;24(1):26. doi: 10.1186/s12885-023-11766-6.

Abstract

Background: Epigenetic alterations contribute greatly to the development and progression of colorectal cancer, and effect of aberrant miR-622 expression is still controversial. This study aimed to discover miR-622 regulation in CRC proliferation.

Methods: miR-622 expression and prognosis were analyzed in clinical CRC samples from Nanfang Hospital. miR-622 regulation on cell cycle and tumor proliferation was discovered, and FOLR2 was screened as functional target of miR-622 using bioinformatics analysis, which was validated via dual luciferase assay and gain-of-function and loss-of-function experiments both in vitro and in vivo.

Results: miR-622 overexpression in CRC indicated unfavorable prognosis and it regulated cell cycle to promote tumor growth both in vitro and in vivo. FOLR2 is a specific, functional target of miR-622, which negatively correlates with signature genes in cell cycle process to promote CRC proliferation.

Conclusions: miR-622 upregulates cell cycle process by targeting FOLR2 to promote CRC proliferation, proposing a novel mechanism and treatment target in CRC epigenetic regulation of miR-622.

Keywords: Cell cycle; Colorectal cancer; FOLR2; Proliferation; miR-622.

MeSH terms

  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation* / genetics
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • Epigenesis, Genetic
  • Folate Receptor 2* / genetics
  • Folate Receptor 2* / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs* / metabolism

Substances

  • Folate Receptor 2
  • FOLR2 protein, human
  • MicroRNAs
  • MIRN622 microRNA, human