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China Pharmacy ; (12): 2827-2831, 2021.
Article in Chinese | WPRIM | ID: wpr-906647

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.

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