Effects and Mechanism of Oncolytic Virus M 1 Inducing the Apoptosis of Cervical Cancer C- 33A Cells
- VernacularTitle:溶瘤病毒M1诱导宫颈癌细胞C-33A凋亡的作用及机制
- Author:
Xiao XIAO
1
;
Yasi ZHOU
2
;
Chuyin PENG
1
;
Jinqing DENG
2
;
Laiyou WANG
1
;
Wenbo ZHU
3
Author Information
1. Dept. of Pharmacy，Guangdong Provincial People’s Hospital/Guangdong Academy of Medical Sciences，Guangzhou 510080，China
2. School of Pharmacy，Guangdong Pharmaceutical University，Guangzhou 510006，China
3. Dept. of Pharmacology，Zhongshan School of Medicine，Sun Yat-sen University，Guangzhou 510080，China
- Publication Type:Journal Article
- Keywords:
Oncolytic virus M 1;
Cervical cancer;
C-33A cells;
Endoplasmic reticulum stress;
Cell apoptosis
- From:
China Pharmacy
2021;32(23):2827-2831
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE：To study the effects and mechanism of oncolytic virus M 1（called M 1 virus for short ）inducing the apoptosis of cervical cancer C-33A cells. METHODS ：MTT assay was used to detect survival rate of C- 33A cells that were treated with different titers （0，0.001，0.01，0.1，1，10 PFU/cell）of M 1 virus. C- 33A cells were divided into control group （0 PFU/cell）， low-dose，medium-dose and high-dose groups of M 1 virus（0.001，0.01，0.1 PFU/cell）. After treated with corresponding titers of M1 virus for 48 h，flow cytometry was used to detect the apoptotic rate and infection rate of cells；Western blot was performed to detect the protein expression of C/EBP homologous proteins （CHOP），caspase-12，caspase-3 and cleaved-caspase- 3. RESULTS ： After treated with different titers of M 1 virus，the survival rate of C- 33A cells decreased significantly （P＜0.01），and showed a dose-dependent tr end. Compared with control group ，the apoptotic rate and infection rate of cells in M 1 virus groups as well as the protein expression of CHOP ，caspase-12 and cleaved-caspase- 3（except for medium-dose group ）in M 1 virus medium-dose and high-dose groups were increased significantly （P＜0.01）. CONCLUSIONS ：M1 virus can induce the apoptosis of cervical cancer C-33A cells ，and its mechanism may be related to the activation of endoplasmic reticulum stress pathway.
