ATPase copper transporter A, negatively regulated by miR-148a-3p, contributes to cisplatin resistance in breast cancer cells.
ATP7A
breast cancer
chemoresistance
cisplatin
miR-148a-3p
Journal
Clinical and translational medicine
ISSN: 2001-1326
Titre abrégé: Clin Transl Med
Pays: United States
ID NLM: 101597971
Informations de publication
Date de publication:
Jan 2020
Jan 2020
Historique:
received:
17
03
2020
accepted:
18
03
2020
entrez:
9
6
2020
pubmed:
9
6
2020
medline:
9
6
2020
Statut:
ppublish
Résumé
Breast cancer is the leading cause of death among women. Cisplatin is an effective drug for breast cancer, but resistance often develops during long term chemotherapy. While the mechanism of chemotherapy resistance is still not fully understood. Survival analyses of ATP7A and ATP7B were used to evaluate their effects on the development of Breast invasive carcinoma (BRCA). Immunostaining, flow cytometry, and IC50 assay were utilized to examine the effects of ATP7A-siRNA combined with cisplatin on apoptosis in breast cancer cells. Q-PCR, western blotting, and dual-luciferase assay were employed to confirm ATP7A is a novel target gene of miR-148a-3p. In this current study, we identified knocking-down ATP7A could enhance cytotoxicity treatment of cisplatin in breast cancer cells. We also demonstrated miR-148a-3p overexpression in BRCA cells increased the sensitivity to cisplatin, and subsequently enhanced DNA damage and apoptosis. Moreover, we found ATP7A is a novel target gene of miR-148a-3p. In brief, our results showed miR-148a could accelerate chemotherapy induced-apoptosis in breast cancer cells by inhibiting ATP7A expression. Our results highlight that inhibition of ATP7A is a potential strategy for targeting breast cancer resistant to cisplatin, and we provided an interesting method to compare the involvement of various genes in the assessment of cisplatin resistance.
Sections du résumé
BACKGROUND
BACKGROUND
Breast cancer is the leading cause of death among women. Cisplatin is an effective drug for breast cancer, but resistance often develops during long term chemotherapy. While the mechanism of chemotherapy resistance is still not fully understood.
METHODS
METHODS
Survival analyses of ATP7A and ATP7B were used to evaluate their effects on the development of Breast invasive carcinoma (BRCA). Immunostaining, flow cytometry, and IC50 assay were utilized to examine the effects of ATP7A-siRNA combined with cisplatin on apoptosis in breast cancer cells. Q-PCR, western blotting, and dual-luciferase assay were employed to confirm ATP7A is a novel target gene of miR-148a-3p.
RESULTS
RESULTS
In this current study, we identified knocking-down ATP7A could enhance cytotoxicity treatment of cisplatin in breast cancer cells. We also demonstrated miR-148a-3p overexpression in BRCA cells increased the sensitivity to cisplatin, and subsequently enhanced DNA damage and apoptosis. Moreover, we found ATP7A is a novel target gene of miR-148a-3p. In brief, our results showed miR-148a could accelerate chemotherapy induced-apoptosis in breast cancer cells by inhibiting ATP7A expression.
CONCLUSIONS
CONCLUSIONS
Our results highlight that inhibition of ATP7A is a potential strategy for targeting breast cancer resistant to cisplatin, and we provided an interesting method to compare the involvement of various genes in the assessment of cisplatin resistance.
Identifiants
pubmed: 32508020
doi: 10.1002/ctm2.19
pmc: PMC7240853
doi:
Types de publication
Journal Article
Langues
eng
Pagination
57-73Subventions
Organisme : Heilongjiang Province Scientific Research Institution Innovation Grants
ID : YC2016D002
Informations de copyright
© 2020 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.
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