Abstract

Hepatocellular carcinoma is one of the most prevalent and lethal cancers with limited therapeutic options. Pathogenesis of this disease involves tumor hypoxia and the activation of hypoxia inducible factors. In this review, we describe the current understanding of hypoxia signaling pathway and summarize the expression, function and target genes of hypoxia inducible factors in hepatocellular carcinoma. We also highlight the recent progress in hypoxia-targeted therapeutic strategies in hepatocellular carcinoma and discuss further the future efforts for the study of hypoxia and/or hypoxia inducible factors in this deadly disease.

Highlights

  • Hepatocellular carcinoma (HCC) is the most common form of liver cancer (70%–90%)

  • We describe the current understanding of hypoxia signaling pathway and summarize the expression, function and target genes of hypoxia inducible factors in hepatocellular carcinoma

  • Combination of antisense HIF1α and B7-1-mediated immunotherapy led to a strong synergistic effect in inducing NK cell- and CD8 T cell-dependent rejection of larger EL-4 tumors (0.4 cm in diameter) [112], highlighting the promise of targeting hypoxia pathway together with cancer immunotherapy in HCC treatment

Read more

Summary

Introduction

Hepatocellular carcinoma (HCC) is the most common form of liver cancer (70%–90%). As the 2nd leading cause of global cancer mortality, HCC endangers over 780,000 new patients per year [1]. We describe the current understanding of hypoxia signaling pathway and summarize the expression, function and target genes of hypoxia inducible factors in hepatocellular carcinoma. Hypoxia inducible factors (HIFs) are critical to sense intratumoral oxygen tension and mediate subsequently the activation of hypoxia response, representing as potential anti-cancer targets [10].

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.