ArticleMedical oncology (Northwood, London, England)2008
E1A inhibits the proliferation of human cervical cancer cells (HeLa cells) by apoptosis induction through activation of HER-2/Neu/Caspase-3 pathway.
Article in Medical oncology (Northwood, London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The Effect of PEI-Mediated E1A on the Radiosensitivity of Hepatic Carcinoma Cells.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Twist1-induced epithelial-mesenchymal transition according to microsatellite instability status in colon cancer cells.Oncotarget · 2016Article
- The interrelationship between HER2 and CASP3/8 with apoptosis in different cancer cell lines.Molecular biology reports · 2014Article
- CD133(+)EpCAM(+) phenotype possesses more characteristics of tumor initiating cells in hepatocellular carcinoma Huh7 cells.International journal of biological sciences · 2012Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study is to investigate the inhibitory effect of E1A gene on the cell proliferation of HeLa cells and its mechanism related to apoptosis.
methodsMTT assay and soft agar colony formation assay were employed to justify the inhibition activity of E1A on the proliferation of HeLa cells transfected with E1A gene. Western Blot, RT-PCR and Real-time quantitative RT-PCR were used to detect the gene expression of E1A, HER-2/Neu and Caspase-3 in HeLa cells, respectively. The Caspase-3 activity was monitored by ApoAlert Caspase-3 Assay. The redistribution of cell cycles and apoptosis of HeLa cells regulated by E1A expression were evaluated by flow cytometry.
resultsE1A expression significantly inhibits the cell proliferation and anchorage-independent cell growth of HeLa, with the respective highest inhibition rate of 40.7% and 43.4% (P < 0.01). HER-2/Neu expression in HeLa was significantly down-regulated by E1A, while the protein expression and activity of Caspase-3 was up-regulated by E1A expression. Flow cytometry revealed that E1A transfection in HeLa increased the cell number at G1 stage and simultaneously decreased the cell number at S stage. E1A transfection induced 8.71% of HeLa cells at apoptosis status.
conclusionsE1A significantly inhibits the cell proliferation of HeLa by the apoptosis induction through HER-2/Neu/Caspase-3 pathway. These results encourage us to continue an in-vivo study and preclinical development of LPD-E1A as a novel gene therapeutic agent for human cervical cancer.
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