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Copper/MYC/CTR1 interplay: a dangerous relationship in hepatocellular carcinoma
Cristiana Porcu1,2, Laura Antonucci1,2, Barbara Barbaro1,2
1MESVA Department, University of L'Aquila, L'Aquila, Italy.
Oncotarget
|March 7, 2018
Summary
Elevated serum copper levels are linked to liver cancer progression. This study reveals how copper, through the MYC/CTR1 pathway, enhances liver cancer cell growth and invasion, offering new diagnostic and therapeutic targets.
Area of Science:
- Hepatocellular Carcinoma Research
- Molecular Biology
- Oncology
Background:
- Serum copper levels correlate with cancer incidence and progression, particularly hepatocellular carcinoma (HCC).
- Non-alcoholic fatty liver disease (NAFLD) progression to HCC is linked to inadequate copper levels.
- MYC oncogene overexpression is common in HCC and drives tumor growth and metastasis.
Purpose of the Study:
- To investigate the role of elevated serum copper in the progression of NAFLD-cirrhosis to HCC.
- To determine if high copper levels sensitize liver cells to transformation.
- To explore the interplay between copper-related proteins and the MYC oncogene.
Main Methods:
- Analysis of serum copper levels in NAFLD-cirrhotic and HCC patients.
- Investigating the effect of high extracellular copper on liver cancer cell growth, migration, and invasion.
- Examining the interaction between MYC and the CTR1 promoter using molecular biology techniques.
Main Results:
- NAFLD-cirrhotic and HCC patients exhibited significantly higher serum copper levels, with the highest in HCC patients.
- High extracellular copper concentrations promoted liver cancer cell growth, migration, and invasion.
- MYC was found to bind the CTR1 promoter, regulating its transcription, with both CTR1 and MYC expression increasing from NAFLD-cirrhosis to HCC.
Conclusions:
- Copper, MYC, and CTR1 form an interplay that promotes liver cancer progression from cirrhosis.
- This Cu/MYC/CTR1 axis offers potential for improved HCC diagnosis and novel combination therapies.
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