Oxycodone enhances antitumor effect of paclitaxel on human breast cancer SKBR3 cells in vitro
Clinics
; Clinics;79: 100458, 2024. graf
Article
em En
|
LILACS-Express
| LILACS
| ID: biblio-1574748
Biblioteca responsável:
BR1.1
ABSTRACT
Abstract Background:
The influences of Oxycodone (OXY) combined with Paclitaxel (PTX) on breast cancer cells are unclear. The present study aimed to examine the effects of OXY combined with PTX on the proliferation, apoptosis, and migration of human breast cancer SKBR3 cells and the underlying mechanism.Methods:
The proliferation, apoptosis and invasion of SKBR3 cells were assessed by CCK-8, colony formation assay, flowcytometric, Transwell assay and scratch assays, respectively. In addition, Western blotting was used to detect the expression of related proteins in these cells. The autophagic bodies were observed under a transmission electron microscope.Results:
OXY (0.25, 0.5 and 1 mM) significantly inhibited the viability, colony-forming, migration, and invasion of SKBR3 cells as compared to the control group. Furthermore, OXY (0.25, 0.5 and 1 mM) markedly induced the apoptosis of SKBR3 cells and the levels of apoptosis-related proteins. In addition, OXY (0.25, 0.5 and 1 mM) and PTX inhibited the proliferation of SKBR3 cells synergistically as compared to PTX group in vitro. Moreover, OXY (0.25, 0.5 and 1 mM) significantly elevated the PTX-induced apoptosis in SKBR3 cells via downregulating the expression of N-cadherin, Becline-1 LC3-II, p-Akt and p-mTOR and upregulating E-cadherin expression. Compared with the control group, OXY (1 mM) treatment induced autophagy in SKBR3 cells.Conclusions:
The present study indicates that OXY can enhance the antitumor effect of PTX on breast cancer in vitro. Hence, the combination of OXY with PTX may serve as a potential strategy for the treatment of breast cancer.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Idioma:
En
Revista:
Clinics
Assunto da revista:
MEDICINA
Ano de publicação:
2024
Tipo de documento:
Article
/
Project document
País de afiliação:
China
País de publicação:
Brasil