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MYC determines lineage commitment in KRAS-driven primary liver cancer development.

Luana D'Artista1, Athina Anastasia Moschopoulou1, Iros Barozzi2

  • 1Department of Medical Oncology and Pneumology (Internal Medicine VIII), University Hospital Tuebingen, Tuebingen, Germany; iFIT Cluster of Excellence EXC 2180 'Image Guided and Functionally Instructed Tumor Therapies', University of Tuebingen, Tuebingen, Germany.

Journal of Hepatology
|March 11, 2023
PubMed
Summary
This summary is machine-generated.

The oncogenic master regulator MYC acts as a switch between hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA) in primary liver cancer (PLC). MYC levels determine whether a transformed liver cell develops into HCC or iCCA.

Keywords:
CancerCell of originHepatocellular carcinoma (HCC)HepatocyteIntrahepatic cholangiocarcinoma (iCCA)LiverMYC

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Primary liver cancer (PLC) includes hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), differing in biology and treatment response.
  • Liver cells possess plasticity, capable of forming either HCC or iCCA, but intrinsic mechanisms of lineage commitment remain unclear.

Purpose of the Study:

  • To identify cell-intrinsic factors that determine lineage commitment in primary liver cancer.
  • To elucidate the molecular mechanisms differentiating HCC from iCCA development.

Main Methods:

  • Applied cross-species transcriptomic and epigenetic profiling to murine and human PLC samples.
  • Utilized integrative bioinformatic analyses including LISA and HOMER.
  • Conducted functional genetic testing in genetically engineered mouse models of PLC.

Main Results:

  • Identified transcription factors FOXA1 and FOXA2 as MYC-dependent determinants of the HCC lineage.
  • Identified ETS1 as a determinant of the iCCA lineage, suppressed by MYC during HCC development.
  • Demonstrated that manipulating FOXA1/FOXA2 and ETS1 expression can switch HCC to iCCA development in mouse models.

Conclusions:

  • Established MYC as a key determinant of lineage commitment in primary liver cancer.
  • Provided a molecular explanation for how liver-damaging factors can lead to either HCC or iCCA.
  • Highlighted potential therapeutic implications for primary liver cancer treatment.