ArticleGene therapy2011
E-cadherin contributes to the bystander effect of TK/GCV suicide therapy and enhances its antitumoral activity in pancreatic cancer models.
Article in Gene therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Adherens junction protein expression is associated with poor response to neoadjuvant FLOT chemotherapy and pro-inflammatory tumor microenvironment in esophageal adenocarcinoma.International journal of cancer · 2026Article
- The Therapeutic Role of NPS-1034 in Pancreatic Ductal Adenocarcinoma as Monotherapy and in Combination with Chemotherapy.International journal of molecular sciences · 2024Article
- Split genome-based retroviral replicating vectors achieve efficient gene delivery and therapeutic effect in a human glioblastoma xenograft model.BMB reports · 2022Article
- Role of Extracellular Vesicles in Compromising Cellular Resilience to Environmental Stressors.BioMed research international · 2021Review
- Suicide Gene Therapy By Amphiphilic Copolymer Nanocarrier for Spinal Cord Tumor.Nanomaterials (Basel, Switzerland) · 2019Article
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- Basolateral CD147 induces hepatocyte polarity loss by E-cadherin ubiquitination and degradation in hepatocellular carcinoma progress.Hepatology (Baltimore, Md.) · 2018Article
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- Gene-directed enzyme prodrug therapy.The AAPS journal · 2015Review
- Polarity proteins as regulators of cell junction complexes: implications for breast cancer.Pharmacology & therapeutics · 2013Review
- Intraductal delivery of adenoviruses targets pancreatic tumors in transgenic Ela-myc mice and orthotopic xenografts.Oncotarget · 2013Article
- Improved retroviral suicide gene transfer in colon cancer cell lines after cell synchronization with methotrexate.Journal of experimental & clinical cancer research : CR · 2011Article
- Antitumor activity of mutant bacterial cytosine deaminase gene for colon cancer.World journal of gastroenterology · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The thymidine kinase/ganciclovir (TK/GCV) cancer gene therapy approach is based on inducing GCV metabolite cytotoxicity in tumor cells expressing the herpes simplex virus TK gene and exposed to GCV. A bystander effect, mediated by gap junctions, accounts for the transfer of toxic metabolites from TK-expressing cells to neighboring cells. It has been proposed that E-cadherin participates in the formation and function of such gap junctions. In this study we investigate the influence of E-cadherin on TK/GCV suicide therapy with a panel of cellular and in vivo models of pancreatic ductal adenocarcinoma. We observed a strong correlation of E-cadherin expression and the TK/GCV bystander effect, associated with the modulation of gap junction communication and connexin expression or localization. Importantly, the co-expression of TK and E-cadherin genes in the adenoviral vector AdTat8TKIE improved TK/GCV cytotoxicity and triggered a potent antitumoral effect, superior to standard AdTat8TK/GCV in MIAPaCa-2 xenografts. The increased expression of E-cadherin resulted in the reduction of the bcl-2 content. Interestingly, the knockdown of bcl-2 sensitized cells to TK/GCV. Thus, we propose that by restoring E-cadherin in pancreatic tumor cells we will improve TK/GCV therapy, both by enhancing the bystander effect and by facilitating the induction of apoptosis.
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