These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Enforced expression of a truncated form of Bax-alpha (tBax) driven by human telomerase reverse transcriptase (hTERT) promoter sensitizes tumor cells to chemotherapeutic agents or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
    Author: Toyota H, Kondo S, Kyo S, Mizuguchi J.
    Journal: Anticancer Res; 2006; 26(1A):99-105. PubMed ID: 16475685.
    Abstract:
    BACKGROUND: We have recently demonstrated that a truncated form of the pro-apoptotic molecule Bax-alpha (tBax) at the NH2-terminus is more potent in inducing cell death than wild-type (wt) Bax. In the present study, whether efficient cell death is induced by tBax expression from human telomerase reverse transcriptase (hTERT) promoter, which is highly active in tumor but not normal cells, was examined. MATERIALS AND METHODS: Cell death was assessed by luciferase reporter assay and the annexin staining method. RESULTS: Enforced expression of tBax resulted in cell death to a greater extent than wt Bax in two types of tumor cells: osteogenic sarcoma MG-63 and squamous cell carcinoma MIT7. The tBax sensitized these tumor cells to death induced by chemotherapeutic agents. Moreover, tBax enhanced cell death induced by the tumor necrosis factor-related apoptosis-inducing ligand to a high level, compared with wt Bax. Furthermore, tBax efficiently induced death of the MG-63 cells overexpressing Bcl-x(L), compared with wt Bax. CONCLUSION: tBax alone, or in combination with chemotherapeutic agents, would be a promising candidate for human gene therapy in the setting of carcinoma, especially for tumors containing high levels of Bcl-x(L).
    [Abstract] [Full Text] [Related] [New Search]