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Title 

HPV E6 antisense induces apoptosis in CaSki cells via suppression of E6 splicing

Authors 

Cheong Weon ChoHa Ryoung PooYoung Sik ChoMin Chul ChoKyung-Ae LeeShin Je LeeSue Nie ParkIn Ki KimYong Keun JungYong Kyung ChoeYoung Il YeomIn Seong ChoeDo Young Yoon

Publisher 

Korean Society of Medical Biochemistry

Issue Date 

2002

Citation 

Experimental and Molecular Medicine, vol. 34, no. 2, pp. 159-166

Keywords 

antisenseapoptosiscaspasecytochrome cE6 splicingmitochodrial potential transitionHPV E6p53E6 protein, human papillomavirus type 16cancer cell culture

Abstract 

Cervical cancer is known to be highly associated with viral oncogene E6 and E7 of human papilloma virus. Down-regulation of oncogene expression by antisense-based gene therapy has been extensively studied. To investigate the effect of HPV 16 E6 antisense nucleic acid (AS) on cervical cancer cells, human cervical cancer cell lines, CaSki and SiHa cells harboring HPV 16 genome were transfected with plasmid containing E6(AS). The decreased viability and the apoptotic morphology were observed in E6(AS)-transfected cervical cancer cell lines. By 6 h after transfection, inhibition of E6 splicing, rapid upregulations of p53 and a p53-responsive protein, GADD45, were displayed in E6(AS)-transfected CaSki cells. Furthermore, E6(AS) induced loss of mitochondrial transmembrane potential, release of mitochondrial cytochrome c into the cytoplasm, and subsequent activation of caspase-9 and caspase-3. These results indicate that HPV 16 E6(AS) induces apoptosis in CaSki cells via upregulation of p53 and release of cytochrome c into cytoplasm, consequently activating procaspase-9 and procaspase-3.

ISSN 

1226-3613

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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