| Full text | |
| Author(s): Show less - |
Carrillo-Beltran, Diego
[1]
;
Munoz, Juan P.
[2]
;
Guerrero-Vasquez, Nahir
[1]
;
Blanco, Rances
[1]
;
Leon, Oscar
[3]
;
de Souza Lino, Vanesca
[4]
;
Tapia, Julio C.
[5]
;
Maldonado, Edio
[5]
;
Dubois-Camacho, Karen
[6]
;
Hermoso, Marcela A.
[6]
;
Corvalan, Alejandro H.
[7, 8]
;
Calaf, Gloria M.
[2, 9]
;
Boccardo, Enrique
[4]
;
Aguayo, Francisco
[8, 1]
Total Authors: 14
|
| Affiliation: | [1] Univ Chile, Fac Med, Inst Ciencias Biomed ICBM, Programa Virol, Lab Oncovirol, Santiago 8380000 - Chile
[2] Univ Tarapaca, Inst Alta Invest, Arica 1000000 - Chile
[3] Univ Lagos, Dept Acuicultura & Recursos Agroalimentarios, Osorno 933 - Chile
[4] Univ Sao Paulo, Inst Biomed Sci, Dept Microbiol, BR-05508900 Sao Paulo - Brazil
[5] Univ Chile, Fac Med, Inst Ciencias Biomed ICBM, Programa Biol Celular & Mol, Santiago 8380000 - Chile
[6] Univ Chile, Fac Med, Inst Ciencias Biomed, Immunol Program, Innate Immun Lab, Santiago 8380000 - Chile
[7] Pontificia Univ Catolica Chile, Sch Med, Hematol & Oncol Dept, Santiago 8330024 - Chile
[8] Pontificia Univ Catolica Chile, Adv Ctr Chron Dis ACCDiS, Santiago 8330024 - Chile
[9] Columbia Univ, Ctr Radiol Res, Med Ctr, New York, NY 10032 - USA
Total Affiliations: 9
|
| Document type: | Journal article |
| Source: | CANCERS; v. 12, n. 7 JUL 2020. |
| Web of Science Citations: | 0 |
| Abstract | |
A subset of oral carcinomas is etiologically related to high-risk human papillomavirus (HR-HPV) infection, with HPV16 being the most frequent HR-HPV type found in these carcinomas. The oncogenic role of HR-HPV is strongly dependent on the overexpression of E6 and E7 oncoproteins, which, in turn, induce p53 and pRb degradation, respectively. Additionally, it has been suggested that HR-HPV oncoproteins are involved in the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), inducing cancer progression and metastasis. Previously, we reported that HPV16 E7 oncoprotein promotes Pirin upregulation resulting in increased epithelial-mesenchymal transition (EMT) and cell migration, with Pirin being an oxidative stress sensor and activator of NF-kappa B. In this study, we demonstrate the mechanism by which HPV16 E7-mediated Pirin overexpression occurs by promoting EGFR/PI3K/AKT1/NRF2 signaling, thus causing PIR/NF-kappa B activation in oral tumor cells. Our results demonstrate a new mechanism by which E7 contributes to oral cancer progression, proposing PIR as a potential new therapeutic target. (AU) | |
| FAPESP's process: | 17/02997-3 - Role of the protein RECK in HPV-mediated cell transformation |
| Grantee: | Enrique Mario Boccardo Pierulivo |
| Support Opportunities: | Regular Research Grants |
| FAPESP's process: | 10/20002-0 - Study of Synthetic Lethality in cells infected with Human Papillomaviruses (HPV) |
| Grantee: | Enrique Mario Boccardo Pierulivo |
| Support Opportunities: | Research Grants - Young Investigators Grants |