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CSN6-SPOP-HMGCS1 Axis Promotes Hepatocellular Carcinoma Progression via YAP1 Activation.

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  • 1Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510655, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 2, 2024
PubMed
Summary

This study reveals CSN6 promotes liver cancer by stabilizing HMGCS1, which activates YAP1. Targeting CSN6 and HMGCS1 inhibits tumor growth, offering a new strategy for fatty liver disease-associated cancers.

Keywords:
HFDYAP1cholesterol metabolismhepatocellular carcinoma(HCC)

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Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Cholesterol metabolism is crucial for cell membrane integrity and implicated in diseases like obesity and cancer.
  • Cancer cells exhibit high cholesterol synthesis for proliferation and microenvironment modulation, yet targeting this pathway is challenging.
  • Hepatocellular carcinoma (HCC) progression is linked to dysregulated metabolic processes.

Purpose of the Study:

  • To investigate the role of CSN6 in hepatocellular carcinoma (HCC) pathogenesis.
  • To elucidate the molecular mechanism by which CSN6 influences cholesterol metabolism and tumor growth.
  • To evaluate the therapeutic potential of targeting the CSN6-HMGCS1-YAP1 axis in HCC.

Main Methods:

  • Analysis of CSN6 expression in HCC tissues.
  • Investigation of the interaction between CSN6, HMGCS1, and SPOP using biochemical assays.
  • Assessment of HMGCS1 stabilization by CSN6 and its effect on YAP1 activation.
  • Evaluation of therapeutic efficacy of targeting CSN6 and HMGCS1 in orthotopic liver cancer models and patient-derived xenografts.

Main Results:

  • CSN6 is upregulated in HCC and positively regulates hydroxymethylglutaryl-CoA synthase 1 (HMGCS1) in the mevalonate pathway.
  • CSN6 antagonizes SPOP ubiquitin ligase, leading to HMGCS1 stabilization and subsequent YAP1 activation, promoting tumor growth.
  • Inhibition of CSN6 and HMGCS1 effectively hinders tumor growth in preclinical HCC models, irrespective of diet.
  • HMGCS1 depletion enhances the efficacy of YAP inhibitors in patient-derived xenografts.

Conclusions:

  • A novel CSN6-HMGCS1-YAP1 signaling axis drives tumor outgrowth in HCC.
  • Targeting CSN6 and HMGCS1 presents a promising therapeutic strategy for HCC, particularly in the context of non-alcoholic fatty liver disease.
  • This axis offers a potential therapeutic target for improving outcomes in HCC patients.