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

Cheong Weon Cho1, Haryoung Poo, Young Sik Cho

  • 1Division of Life Sciences, Korea Research Institute of Bioscience and Biotechnology, Yuseong, Taejon.

Experimental & Molecular Medicine
|June 29, 2002
PubMed

Insights

Antisense nucleic acid targeting human papillomavirus (HPV) 16 E6 oncogene effectively reduced cervical cancer cell viability and induced apoptosis. This therapy upregulates p53, triggers mitochondrial dysfunction, and activates caspases, offering a potential gene therapy strategy for cervical cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Cervical cancer is strongly linked to human papillomavirus (HPV) oncogenes E6 and E7.
  • Antisense-based gene therapy is a studied approach to down-regulate oncogene expression.

Purpose of the Study:

  • To investigate the impact of HPV 16 E6 antisense nucleic acid (AS) on cervical cancer cells.
  • To explore the molecular mechanisms of E6(AS) in inducing cancer cell death.

Main Methods:

  • Transfection of CaSki and SiHa cervical cancer cell lines with a plasmid encoding E6(AS).
  • Analysis of cell viability, apoptotic morphology, E6 splicing, p53 and GADD45 expression.
  • Assessment of mitochondrial transmembrane potential, cytochrome c release, and caspase activation.

Main Results:

  • E6(AS) transfection led to decreased viability and apoptotic morphology in cervical cancer cells.
  • Inhibition of E6 splicing and rapid upregulation of p53 and GADD45 were observed.
  • E6(AS) induced mitochondrial dysfunction, cytochrome c release, and activation of caspase-9 and caspase-3.

Conclusions:

  • HPV 16 E6(AS) effectively induces apoptosis in cervical cancer cells.
  • The mechanism involves p53 upregulation and mitochondrial pathway activation, including cytochrome c release and caspase cascade initiation.

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