miR-22 Suppresses EMT by Mediating Metabolic Reprogramming in Colorectal Cancer through Targeting MYC-Associated

Shusen Xia1,2,3, Xianyan Wang4, Yi Wu1,2

  • 1The Second Department of General Surgery, The Affiliated Hospital of the North Sichuan Medical College, Nanchong, 637000 Sichuan, China.

Disease Markers
|September 5, 2022
PubMed

Insights

MicroRNA-22 (miR-22) acts as a tumor suppressor in colorectal cancer (CRC) by targeting MAX. Downregulation of miR-22 promotes CRC progression, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Colorectal cancer (CRC) is a prevalent gastrointestinal malignancy.
  • MicroRNAs (miRNAs) exhibit altered expression in CRC, influencing cellular processes.
  • The specific role of microRNA-22 (miR-22) in CRC remains incompletely understood.

Purpose of the Study:

  • To investigate the expression, function, and mechanism of miR-22 in colorectal cancer.
  • To determine the relationship between miR-22 and MYC-associated factor X (MAX) in CRC.
  • To explore the potential of miR-22 as a therapeutic target for CRC.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for gene expression analysis.
  • Luciferase reporter and coimmunoprecipitation assays for target validation.
  • Gain- and loss-of-function studies in CRC cells and a mouse xenograft model.

Main Results:

  • miR-22 was found to be hypermethylated and downregulated in CRC tissues and cells.
  • MAX expression was upregulated in CRC.
  • miR-22 inhibited CRC cell migration, invasion, glycolysis, and cancer stem cell transcription factors by directly targeting MAX.

Conclusions:

  • miR-22 functions as a tumor suppressor in colorectal cancer.
  • The miR-22/MAX axis plays a critical role in CRC progression.
  • Targeting miR-22 may offer a novel therapeutic strategy for colorectal cancer.

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