TY - JOUR
T1 - The Molecular Interplay between Human Oncoviruses and Telomerase in Cancer Development
AU - Tornesello, Maria Lina
AU - Cerasuolo, Andrea
AU - Starita, Noemy
AU - Tornesello, Anna Lucia
AU - Bonelli, Patrizia
AU - Tuccillo, Franca Maria
AU - Buonaguro, Luigi
AU - Isaguliants, Maria G.
AU - Buonaguro, Franco M.
N1 - Funding Information:
This work was supported by the Italian Ministry of Health Ricerca Corrente 2022 Grant L1/10. M.I. Isaguliants was supported by the Latvian Science Fund, project LZP 2021/1-0484.
Publisher Copyright:
© 2022 by the authors.
PY - 2022/10/26
Y1 - 2022/10/26
N2 - Human oncoviruses are able to subvert telomerase function in cancer cells through multiple strategies. The activity of the catalytic subunit of telomerase (TERT) is universally enhanced in virus-related cancers. Viral oncoproteins, such as high-risk human papillomavirus (HPV) E6, Epstein–Barr virus (EBV) LMP1, Kaposi’s sarcoma-associated herpesvirus (HHV-8) LANA, hepatitis B virus (HBV) HBVx, hepatitis C virus (HCV) core protein and human T-cell leukemia virus-1 (HTLV-1) Tax protein, interact with regulatory elements in the infected cells and contribute to the transcriptional activation of TERT gene. Specifically, viral oncoproteins have been shown to bind TERT promoter, to induce post-transcriptional alterations of TERT mRNA and to cause epigenetic modifications, which have important effects on the regulation of telomeric and extra-telomeric functions of the telomerase. Other viruses, such as herpesviruses, operate by integrating their genomes within the telomeres or by inducing alternative lengthening of telomeres (ALT) in non-ALT cells. In this review, we recapitulate on recent findings on virus–telomerase/telomeres interplay and the importance of TERT-related oncogenic pathways activated by cancer-causing viruses.
AB - Human oncoviruses are able to subvert telomerase function in cancer cells through multiple strategies. The activity of the catalytic subunit of telomerase (TERT) is universally enhanced in virus-related cancers. Viral oncoproteins, such as high-risk human papillomavirus (HPV) E6, Epstein–Barr virus (EBV) LMP1, Kaposi’s sarcoma-associated herpesvirus (HHV-8) LANA, hepatitis B virus (HBV) HBVx, hepatitis C virus (HCV) core protein and human T-cell leukemia virus-1 (HTLV-1) Tax protein, interact with regulatory elements in the infected cells and contribute to the transcriptional activation of TERT gene. Specifically, viral oncoproteins have been shown to bind TERT promoter, to induce post-transcriptional alterations of TERT mRNA and to cause epigenetic modifications, which have important effects on the regulation of telomeric and extra-telomeric functions of the telomerase. Other viruses, such as herpesviruses, operate by integrating their genomes within the telomeres or by inducing alternative lengthening of telomeres (ALT) in non-ALT cells. In this review, we recapitulate on recent findings on virus–telomerase/telomeres interplay and the importance of TERT-related oncogenic pathways activated by cancer-causing viruses.
KW - EBV
KW - Epstein–Barr virus
KW - HBV
KW - HCV
KW - hepatitis B virus
KW - hepatitis C virus
KW - HHV-8
KW - HPV
KW - HTLV-1
KW - human papillomavirus
KW - human T-cell leukemia virus-1
KW - Kaposi’s sarcoma-associated herpesvirus
KW - telomerase reverse transcriptase
KW - TERT
KW - TERT promoter
KW - TERTp
UR - http://www.scopus.com/inward/record.url?scp=85141818729&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/1c647a42-4b1d-3cd0-8c43-baa9134139ea/
U2 - 10.3390/cancers14215257
DO - 10.3390/cancers14215257
M3 - Review article
C2 - 36358677
AN - SCOPUS:85141818729
SN - 2072-6694
VL - 14
JO - Cancers
JF - Cancers
IS - 21
M1 - 5257
ER -
