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Review
. 2021 Feb 25;10(3):262.
doi: 10.3390/pathogens10030262.

Human Papillomavirus and Cellular Pathways: Hits and Targets

Alessandro Medda  1 , Daria Duca  1 , Susanna Chiocca  1
Affiliations
Review

Human Papillomavirus and Cellular Pathways: Hits and Targets

Alessandro Medda et al. Pathogens. .

Abstract

The Human Papillomavirus (HPV) is the causative agent of different kinds of tumors, including cervical cancers, non-melanoma skin cancers, anogenital cancers, and head and neck cancers. Despite the vaccination campaigns implemented over the last decades, we are far from eradicating HPV-driven malignancies. Moreover, the lack of targeted therapies to tackle HPV-related tumors exacerbates this problem. Biomarkers for early detection of the pathology and more tailored therapeutic approaches are needed, and a complete understanding of HPV-driven tumorigenesis is essential to reach this goal. In this review, we overview the molecular pathways implicated in HPV infection and carcinogenesis, emphasizing the potential targets for new therapeutic strategies as well as new biomarkers.

Keywords: AP-1; DNA damage response; EGFR; EMT; HPV; JAK/STAT; PI3K/Akt/mTOR; autophagy; cervical cancer; head and neck cancer; miRNA.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Signaling pathways impinged by HPV: (a) HPV E6-mediated degradation of p53; (b) pRb degradation and inactivation by HPV E7; (c) EGFR regulation by HPV E5; (d) PI3K, Akt and mTOR are deregulated by HPV; (e) HPV gene transcription induced by AP-1; (f) Autophagy inhibition by HPV oncoproteins.
Figure 2
Figure 2
EMT and HPV (a) Changes in epithelial and mesenchymal markers induced by HPV; (b) HPV16 E6/E7 inhibit Siah-1 expression and APC activity, leading to β-catenin upregulation.
Figure 3
Figure 3
HPV 16 E6/E7 induce the phosphorylation of STAT-3 and the expression of proliferation, angiogenesis, and tumor growth genes.
See this image and copyright information in PMC

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