Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy

TL;DR

This paper reviews how HPV infection leads to cervical cancer through metabolic changes and hypoxia, and summarizes current therapies.

Contribution

The paper provides a comprehensive overview of the pathogenic mechanisms and therapies for cervical cancer following HPV infection.

Findings

HPV oncoproteins drive metabolic reprogramming in cervical cancer cells, including enhanced glycolysis and altered glutamine and lipid metabolism.

Non-coding RNAs play a role in cervical carcinogenesis mechanisms.

Cancer cells adapt to hypoxic conditions through various survival mechanisms.

Abstract

Cervical cancer has a high incidence and mortality, and is one of the leading causes of cancer-related deaths among women worldwide. The infection with high-risk subtypes of the human papillomavirus (HPV) represents a crucial factor in the development of precancerous lesions. HPV oncoproteins target multiple host factors to promote uncontrolled cellular proliferation, genomic instability, profound metabolic reprogramming, resistance to apoptosis and immune evasion. Thus, cervical carcinogenesis involves metabolic reprogramming in patient cells, such as enhanced aerobic glycolysis, and altered glutamine, lipid and mitochondrial metabolism, which collectively support the bioenergetic and biosynthetic demands of cancer cells. Cancer cells also activate several mechanisms to adapt and survive under hypoxic/anoxic conditions. The mechanisms underlying cervical carcinogenesis often involve non-coding RNAs. This review aims at summarizing the mechanisms and factors involved in the development and progression of cervical cancer following HPV infection, and offers an overview of the available therapies that have been developed for this disease.

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