Inhibition of MID1IP1 induces ferroptosis and suppresses c-Myc expression in colorectal cancer cell

Je Joung Oh1, Yu Jin Lee1, Yeo Jeong Han1

  • 1College of Korean Medicine, Kyung Hee University, Seoul, 02447, Korea.

Genes & Genomics
|December 4, 2025
PubMed
Abstract

Insights

Midline 1 Interacting Protein 1 (MID1IP1) promotes colorectal cancer (CRC) survival by stabilizing c-Myc and preventing ferroptosis. Targeting MID1IP1 may offer new therapeutic strategies for CRC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) is a leading global cancer diagnosis.
  • Drug resistance and metastasis remain significant challenges in CRC treatment.
  • Midline 1 Interacting Protein 1 (MID1IP1) expression correlates with tumor growth via c-Myc.

Purpose of the Study:

  • Investigate MID1IP1's role in CRC metabolic reprogramming.
  • Determine MID1IP1's effect on ferroptosis and cell migration in CRC.
  • Explore the link between MID1IP1, c-Myc, and CRC progression.

Main Methods:

  • MID1IP1 was silenced in HCT116 cells using siRNA.
  • Assays included colony formation, Western blotting, ROS measurement, and wound healing.
  • Proteins assessed included c-Myc, ferroptosis markers, glycolytic enzymes, and EMT markers.

Main Results:

  • MID1IP1 knockdown reduced cell growth and c-Myc stability.
  • Glycolysis and ferroptosis-protective proteins decreased, leading to ROS accumulation and ferroptosis.
  • Cell migration was inhibited, with associated changes in EMT markers.

Conclusions:

  • MID1IP1 enhances CRC cell survival by stabilizing c-Myc and inhibiting ferroptosis.
  • MID1IP1 influences CRC cell migration and metabolic reprogramming.
  • MID1IP1 presents a potential novel biomarker and therapeutic target for CRC.

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