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Effect of simultaneous silencing of HPV-18 E6 and E7 on inducing apoptosis in HeLa cells
Abstract:
The objective of this investigation was to determine if simultaneous silencing of the human papillomavirus type 18 (HPV-18) E6 and E7 oncogenes using RNA interference (RNAi) would be a potential therapeutic approach against the carcinogenic activity of this virus. Two synthetic double-stranded oligonucleotides, encoding short hairpin transcripts corresponding to HPV-18 E6 and E7 genes, were cloned into pGenesilence (pGS) 1.0 vectors to produce pGS-E6, pGS-E7, and pGS-(E6+E7), respectively. Our results showed that the expression of HPV-18 E6 class 1 and HPV-18 E7 in HeLa cells was markedly decreased after being transfected with pGS-E6, pGS-E7, and pGS-(E6+E7) vectors. Of the three vectors, pGS-(E6+E7) had a greater ability to decrease the growth rate of HeLa cells, inhibit colony formation in soft agar, and significantly reduce tumor growth in nude mice. We also found that depletion of HPV-18 E6 and E7 in this manner promoted apoptosis of HeLa cells. Our data showed that simultaneously decreasing HPV-18 E6 and E7 gene expression in HeLa cells by RNAi could significantly inhibit tumor growth under in vitro conditions and in nude mice. These data suggest that gene therapy may be a possible therapeutic approach for HPV-positive cervical cancers.
Insights
Simultaneously silencing human papillomavirus type 18 (HPV-18) E6 and E7 oncogenes with RNA interference (RNAi) effectively inhibited tumor growth in vitro and in vivo. This gene therapy approach shows promise for treating HPV-positive cervical cancers.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Human papillomavirus type 18 (HPV-18) oncogenes E6 and E7 drive cervical cancer development.
- RNA interference (RNAi) offers a potential strategy for targeted gene silencing.
Purpose of the Study:
- To evaluate the therapeutic potential of simultaneously silencing HPV-18 E6 and E7 oncogenes using RNAi.
- To assess the impact of this approach on cancer cell growth, proliferation, and tumor development.
Main Methods:
- Constructed pGS-E6, pGS-E7, and pGS-(E6+E7) vectors for RNAi-mediated gene silencing.
- Transfected HeLa cells with the vectors to decrease HPV-18 E6 and E7 expression.
- Assessed effects on cell growth, colony formation, tumor growth in nude mice, and apoptosis.
Main Results:
- Transfection with pGS vectors significantly reduced HPV-18 E6 and E7 expression in HeLa cells.
- The pGS-(E6+E7) vector demonstrated superior efficacy in inhibiting cell growth and colony formation.
- Simultaneous silencing of E6 and E7 significantly reduced tumor growth in vivo and promoted apoptosis.
Conclusions:
- Simultaneous gene silencing of HPV-18 E6 and E7 via RNAi is a viable therapeutic strategy.
- This approach effectively inhibits tumor growth and induces apoptosis in HPV-positive cancer models.
- Gene therapy targeting HPV oncogenes presents a promising avenue for cervical cancer treatment.
