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c-Myc as a vulnerable target in cancer drug resistance

Milad Ashrafizadeh1

  • 1Department of Radiation Oncology, Shandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.

Gene
|May 30, 2026
PubMed

Insights

The c-MYC proto-oncogene drives cancer treatment resistance through various mechanisms, including metabolic adaptation and immune evasion. Targeting c-MYC offers promising therapeutic strategies to overcome resistance and improve patient outcomes in oncology.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The c-MYC proto-oncogene is a critical regulator of cell growth, metabolism, and apoptosis.
  • c-MYC overexpression is implicated in numerous cancers and confers resistance to various cancer therapies.
  • Understanding c-MYC's role in treatment resistance is crucial for developing effective oncology strategies.

Purpose of the Study:

  • To systematically review the molecular mechanisms by which c-MYC promotes therapeutic resistance.
  • To analyze key signaling pathways involved in c-MYC-mediated resistance.
  • To evaluate current and emerging strategies for targeting c-MYC in cancer treatment.

Main Methods:

  • Comprehensive literature review of studies investigating c-MYC and treatment resistance.
  • Analysis of molecular mechanisms including metabolic adaptation, DNA repair, apoptosis blockade, cancer stem cell maintenance, and immune evasion.
  • Examination of signaling pathways (PI3K/AKT, Wnt/β-catenin, HIF-1α) and regulatory factors (non-coding RNAs, epigenetics, post-translational modifications).

Main Results:

  • c-MYC drives resistance through metabolic reprogramming, enhanced DNA repair, blocked apoptosis, cancer stem cell persistence, and immune evasion.
  • Signaling pathways like PI3K/AKT, Wnt/β-catenin, and HIF-1α are integral to c-MYC-driven resistance.
  • Non-coding RNAs, epigenetic modifications, and post-translational changes contribute to c-MYC stability and therapeutic failure.

Conclusions:

  • Targeting c-MYC through inhibitors or combination therapies holds significant therapeutic potential.
  • Overcoming c-MYC-dependent survival pathways is key to restoring treatment sensitivity.
  • Further understanding of c-MYC's regulatory network can lead to innovative oncology treatments and improved patient outcomes.
Keywords:
ChemoresistanceDrug resistanceMetabolic reprogrammingTargeted therapyc-MYC

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