Human Papillomavirus (HPV) Infection-Associated Epithelial-to-Mesenchymal Transition: Implication in Tumorigenesis and Pathogenesis of HPV-Positive Cancers
- 1Department of Radiation Biochemistry, A. Tsyb Medical Radiological Research Center—Branch of the National Medical Research Radiological Center of the Ministry of Health of the Russian Federation, Koroleva St. 4, 249036 Obninsk, Russia
- 2National Medical Research Radiological Center of the Ministry of Health of the Russian Federation, 249036 Obninsk, Russia
- 3Scientific and Educational Resource Center for Innovative Technologies of Immunophenotyping, Digital Spatial Profiling and Ultrastructural Analysis, Patrice Lumumba Peoples’ Friendship University of Russia (RUDN University), 117198 Moscow, Russia
Abstract
Epithelial-to-mesenchymal transition (EMT) is a programmed and reversible process that allows epithelial cells to temporarily acquire a mesenchymal cell phenotype with increased migratory and invasive capacity. Analogous phenotypic modulation can also occur in carcinoma cells, which, after undergoing EMT, exhibit cancer stem cell-like properties and actively migrate, leading to tumor invasion and metastases. This structured narrative review focuses on the molecular crosstalk between human papillomavirus (HPV) and EMT, which occurs in HPV-infected human epithelium and in HPV-positive cancers of different location (cervical, head and neck, colorectal, lung, and others). The main questions addressed here are: (i) how HPV-driven EMT may contribute to the malignant transformation of HPV-infected epithelial cells, (ii) what mechanistic links may exist between the HPV positivity and EMT in human cancers, and (iii) how EMT in various HPV-positive human tumors may influence their pathogenesis, treatment modalities and outcomes. The relationship between HPV infection and EMT program is delineated as a complex multicomponent mechanism triggered by exogenous and endogenous stimuli and involving specific ligand-receptor interactions, membrane channels, transcription factors, signaling pathways, epigenetic regulators, etc. The review also discusses some of the potential applications of EMT-related biomarkers and molecular targets in the prevention, prediction and treatment of HPV-induced cancers.
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BibTeX
@article{kabakov2026human,
title = {{Human Papillomavirus (HPV) Infection-Associated Epithelial-to-Mesenchymal Transition: Implication in Tumorigenesis and Pathogenesis of HPV-Positive Cancers}},
author = {Alexander E. Kabakov and Olga N. Matchuk and Anna V. Khokhlova and Andrey D. Kaprin},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15201916},
url = {https://www.mdpi.com/2073-4409/15/20/1916},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Human Papillomavirus (HPV) Infection-Associated Epithelial-to-Mesenchymal Transition: Implication in Tumorigenesis and Pathogenesis of HPV-Positive Cancers
AU - Alexander E. Kabakov
AU - Olga N. Matchuk
AU - Anna V. Khokhlova
AU - Andrey D. Kaprin
PY - 2026
DA - 2026/10/21
JO - Cells
DO - 10.3390/cells15201916
UR - https://www.mdpi.com/2073-4409/15/20/1916
AB - Epithelial-to-mesenchymal transition (EMT) is a programmed and reversible process that allows epithelial cells to temporarily acquire a mesenchymal cell phenotype with increased migratory and invasive capacity. Analogous phenotypic modulation can also occur in carcinoma cells, which, after undergoing EMT, exhibit cancer stem cell-like properties and actively migrate, leading to tumor invasion and metastases. This structured narrative review focuses on the molecular crosstalk between human papillomavirus (HPV) and EMT, which occurs in HPV-infected human epithelium and in HPV-positive cancers of different location (cervical, head and neck, colorectal, lung, and others). The main questions addressed here are: (i) how HPV-driven EMT may contribute to the malignant transformation of HPV-infected epithelial cells, (ii) what mechanistic links may exist between the HPV positivity and EMT in human cancers, and (iii) how EMT in various HPV-positive human tumors may influence their pathogenesis, treatment modalities and outcomes. The relationship between HPV infection and EMT program is delineated as a complex multicomponent mechanism triggered by exogenous and endogenous stimuli and involving specific ligand-receptor interactions, membrane channels, transcription factors, signaling pathways, epigenetic regulators, etc. The review also discusses some of the potential applications of EMT-related biomarkers and molecular targets in the prevention, prediction and treatment of HPV-induced cancers.
SN - 2073-4409
ER -