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c-Myc-driven Hepatocarcinogenesis.

Hyuk Moon1, Hyunjung Park1,2, Simon Weonsang Ro3,2

  • 1Department of Genetics and Biotechnology, College of Life Sciences, Kyung Hee University, Gyeonggi-do, Republic of Korea.

Anticancer Research
|October 1, 2021
PubMed
Summary
This summary is machine-generated.

c-Myc drives liver cancer most effectively with activated Ras signaling. P53 inactivation also promotes c-Myc-induced hepatocellular carcinoma (HCC), but other pathway activations did not yield tumors.

Keywords:
Hepatocellular carcinomac-Mycc-MycT58Aoncogenetransgenic

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Dysregulation of the c-Myc gene is a common event in human hepatocellular carcinoma (HCC).
  • Altered c-Myc expression often co-occurs with genetic and epigenetic changes in other cancer-related genes.
  • The role of c-Myc in hepatocarcinogenesis within different genetic contexts is not fully understood.

Purpose of the Study:

  • To investigate the tumorigenic potential of c-Myc in hepatocellular carcinoma (HCC).
  • To determine how c-Myc interacts with activated or inactivated Ras, Wnt/β-catenin, Sonic hedgehog, or P53 pathways in liver cancer development.
  • To assess the impact of c-Myc mutations on hepatocarcinogenesis.

Main Methods:

  • Utilized hydrodynamic tail vein injection to create transgenic mouse models.
  • Administered expression transposons to generate livers expressing c-Myc alongside activated Ras (HRASG12V), β-catenin (β-cateninS33Y), Smo (SmoM2), or P53-targeting shRNA (shp53).
  • Evaluated tumor formation and characterized hepatocellular carcinoma (HCC) development.

Main Results:

  • c-Myc exhibited the highest tumorigenic potential when the RAS signaling pathway was activated.
  • Co-expression of c-Myc with β-cateninS33Y or SmoM2 did not result in tumor formation.
  • Hepatocellular carcinoma (HCC) developed in approximately 40% of mice with c-Myc overexpression and P53 inactivation.
  • No significant difference in tumorigenic potential was observed between wild-type c-Myc and a mutated form (c-MycT58A).

Conclusions:

  • The RAS signaling pathway plays a critical role in potentiating c-Myc-driven hepatocarcinogenesis.
  • P53 inactivation contributes to c-Myc-induced liver cancer.
  • The T58A mutation in c-Myc does not appear to significantly influence its role in hepatocarcinogenesis.