HPV induction of APOBEC3 enzymes mediate overall survival and response to cisplatin in head and neck cancer.
APOBEC Deaminases
Antineoplastic Agents
/ pharmacology
Carboplatin
/ pharmacology
Carcinoma, Squamous Cell
/ drug therapy
Cell Line, Tumor
Cisplatin
/ pharmacology
Cytidine Deaminase
/ metabolism
DNA Mismatch Repair
DNA Repair
Head and Neck Neoplasms
/ drug therapy
Humans
Oxaliplatin
/ pharmacology
Papillomaviridae
APOBEC3
Cisplatin
HPV
Head and neck cancer
Survival
Journal
DNA repair
ISSN: 1568-7856
Titre abrégé: DNA Repair (Amst)
Pays: Netherlands
ID NLM: 101139138
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
06
09
2019
revised:
13
12
2019
accepted:
14
01
2020
pubmed:
26
1
2020
medline:
22
12
2020
entrez:
26
1
2020
Statut:
ppublish
Résumé
Human papillomavirus (HPV) is associated with the development of head and neck squamous cell carcinomas (HNSC). Cisplatin is used to treat HNSC and induces DNA adducts including interstrand crosslinks (ICLs). Previous reports have shown that HPV positive HNSC patients respond better to cisplatin therapy. Our previous reports highlight that loss of base excision repair (BER) and mismatch repair (MMR) results in cisplatin resistance. Of importance, uracil DNA glycosylase (UNG) is required to initiate the BER response to cisplatin treatment and maintain drug sensitivity. These previous results highlight that specific cytidine deaminases could play an important role in the cisplatin response by activating the BER pathway to mediate drug sensitivity. The APOBEC3 (A3) family of cytidine deaminases are enzymes that restrict HPV as part of the immune defense to viral infection. In this study, the Cancer Genome Atlas (TCGA) HNSC data were used to assess the association between the expression of the seven proteins in the A3 cytidine deaminase family, HPV-status and survival outcomes. Higher A3 G expression in HPV-positive tumors corresponds with better overall survival (OS) (HR 0.33, 95 % CI 0.11-0.93, p = 0.04). FaDu and Scc-25 HNSC cell lines were used to assess alterations in A3, BER and MMR expression in response to cisplatin. We demonstrate that A3, Polβ, and MSH6 knockdown in HNSC cells results in resistance to cisplatin and carboplatin as well as an increase in the rate of ICL removal in FaDu and Scc-25 HNSC cells. Our results suggest that A3s activate BER in HNSC, mediate repair of cisplatin ICLs and thereby, sensitize cells to cisplatin which likely contributes to the improved patient responses observed in HPV infected patients.
Identifiants
pubmed: 31981740
pii: S1568-7864(19)30290-3
doi: 10.1016/j.dnarep.2020.102802
pmc: PMC7033022
mid: NIHMS1551613
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Oxaliplatin
04ZR38536J
Carboplatin
BG3F62OND5
APOBEC Deaminases
EC 3.5.4.5
APOBEC3 proteins, human
EC 3.5.4.5
Cytidine Deaminase
EC 3.5.4.5
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
102802Subventions
Organisme : NCI NIH HHS
ID : F31 CA221333
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA229535
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA009531
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare there are no conflicts of interest.
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