Association of BRCA Mutations and BRCAness Status With Anticancer Drug Sensitivities in Triple-Negative Breast Cancer Cell Lines


Journal

The Journal of surgical research
ISSN: 1095-8673
Titre abrégé: J Surg Res
Pays: United States
ID NLM: 0376340

Informations de publication

Date de publication:
06 2020
Historique:
received: 07 10 2019
revised: 02 12 2019
accepted: 26 12 2019
pubmed: 25 2 2020
medline: 22 8 2020
entrez: 25 2 2020
Statut: ppublish

Résumé

Many triple-negative breast cancers (TNBCs) show impaired breast cancer susceptibility gene I (BRCA1) function, called BRCAness. BRCAness tumors may show similar sensitivities to anticancer drugs as tumors with BRCA1 mutations. In this study, we investigated the association of BRCA mutations or BRCAness with drug sensitivities in TNBC. BRCAness was evaluated as BRCA1-like scores, using multiplex ligation-dependent probe amplification in 12 TNBC cell lines, including four with mutations. Sensitivities to docetaxel, cisplatin, and epirubicin were compared with BRCA mutations and BRCA1-like scores. Cisplatin sensitivity was examined in BRCA1 knockdown Michigan Cancer Foundation-7 cell lines. Eight and four cell lines had characteristics of BRCAness and non-BRCAness, respectively. The 50% inhibitory concentration of docetaxel was higher in BRCA mutant and BRCAness cell lines than their counterparts. BRCA1-like scores showed a weak positive correlation with docetaxel sensitivity (r = 0.377; P = 0.039). Regarding cisplatin, scores were lower in BRCA mutants and BRCAness tumors than their counterparts. A negative correlation was found between BRCA1-like scores and cisplatin sensitivity (r = -0.407; P = 0.013). No differences were found for epirubicin. BRCA1 gene knockdown increased the cisplatin sensitivity of Michigan Cancer Foundation-7 cells. BRCA1-like scores were associated with cisplatin sensitivity and docetaxel resistance. BRCA1-like score is hence a promising indicator for estimating drug sensitivities in TNBC.

Sections du résumé

BACKGROUND
Many triple-negative breast cancers (TNBCs) show impaired breast cancer susceptibility gene I (BRCA1) function, called BRCAness. BRCAness tumors may show similar sensitivities to anticancer drugs as tumors with BRCA1 mutations. In this study, we investigated the association of BRCA mutations or BRCAness with drug sensitivities in TNBC.
METHODS
BRCAness was evaluated as BRCA1-like scores, using multiplex ligation-dependent probe amplification in 12 TNBC cell lines, including four with mutations. Sensitivities to docetaxel, cisplatin, and epirubicin were compared with BRCA mutations and BRCA1-like scores. Cisplatin sensitivity was examined in BRCA1 knockdown Michigan Cancer Foundation-7 cell lines.
RESULTS
Eight and four cell lines had characteristics of BRCAness and non-BRCAness, respectively. The 50% inhibitory concentration of docetaxel was higher in BRCA mutant and BRCAness cell lines than their counterparts. BRCA1-like scores showed a weak positive correlation with docetaxel sensitivity (r = 0.377; P = 0.039). Regarding cisplatin, scores were lower in BRCA mutants and BRCAness tumors than their counterparts. A negative correlation was found between BRCA1-like scores and cisplatin sensitivity (r = -0.407; P = 0.013). No differences were found for epirubicin. BRCA1 gene knockdown increased the cisplatin sensitivity of Michigan Cancer Foundation-7 cells.
CONCLUSIONS
BRCA1-like scores were associated with cisplatin sensitivity and docetaxel resistance. BRCA1-like score is hence a promising indicator for estimating drug sensitivities in TNBC.

Identifiants

pubmed: 32092597
pii: S0022-4804(20)30018-4
doi: 10.1016/j.jss.2019.12.040
pii:
doi:

Substances chimiques

Antineoplastic Agents 0
BRCA1 Protein 0
BRCA1 protein, human 0
Docetaxel 15H5577CQD
Cisplatin Q20Q21Q62J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

200-208

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Saeko Teraoka (S)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Masako Muguruma (M)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Naoharu Takano (N)

Department of Biochemistry, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Kana Miyahara (K)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Takahiko Kawate (T)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Hiroshi Kaise (H)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Kimito Yamada (K)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Keisuke Miyazawa (K)

Department of Biochemistry, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.

Takashi Ishikawa (T)

Department of Breast Oncology and Surgery, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan. Electronic address: tishik55@gmail.com.

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Classifications MeSH