Modulation of docetaxel-induced apoptosis and cell cycle arrest by all- trans retinoic acid in prostate cancer cells
2001
Enhancing Docetaxel Toxicity in Prostate Cancer with ATRA
publication
Author Information
Author(s): Nehmé A, Varadarajan P, Sellakumar G, Gerhold M, Niedner H, Zhang Q, Lin X, Christen R D
Primary Institution: Department of Medicine and the Cancer Center, University of California
Hypothesis
Does all-trans retinoic acid enhance the effectiveness of docetaxel in treating prostate cancer cells?
Conclusion
All-trans retinoic acid significantly increases the toxicity of docetaxel in prostate cancer cells by down-regulating Bcl-2 and partially reversing cell cycle arrest.
Supporting Evidence
- All-trans retinoic acid enhanced the toxicity of docetaxel against prostate cancer cells.
- The interaction between ATRA and docetaxel was highly synergistic.
- Docetaxel-induced apoptosis was linked to the inactivation of Bcl-2.
- ATRA inhibited docetaxel-induced phosphorylation of cdc2, reversing G2/M arrest.
- ATRA also inhibited the activation of MAPK related to docetaxel effects.
Takeaway
A special vitamin helped a cancer medicine work better by making cancer cells die more and stopping them from growing.
Digital Object Identifier (DOI)
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