Normal and prostate cancer cells display distinct molecular profiles of α‐tubulin posttranslational modifications

K Souček, A Kamaid, AD Phung, L Kubala… - The …, 2006 - Wiley Online Library
K Souček, A Kamaid, AD Phung, L Kubala, JC Bulinski, RW Harper, JP Eiserich
The Prostate, 2006Wiley Online Library
BACKGROUND Multiple diverse posttranslational modifications of α‐tubulin such as
detyrosination, further cleavage of the penultimate glutamate residue (Δ2‐tubulin),
acetylation, and polyglutamylation increase the structural and functional diversity of
microtubules. METHODS Herein, we characterized the molecular profile of α‐tubulin
posttranslational modifications in normal human prostate epithelial cells (PrEC),
immortalized normal prostate epithelial cells (PZ‐HPV‐7), androgen‐dependent prostate …
BACKGROUND
Multiple diverse posttranslational modifications of α‐tubulin such as detyrosination, further cleavage of the penultimate glutamate residue (Δ2‐tubulin), acetylation, and polyglutamylation increase the structural and functional diversity of microtubules.
METHODS
Herein, we characterized the molecular profile of α‐tubulin posttranslational modifications in normal human prostate epithelial cells (PrEC), immortalized normal prostate epithelial cells (PZ‐HPV‐7), androgen‐dependent prostate cancer cells (LNCaP), transitional androgen‐independent prostate cancer cells (LNCaP‐cds and CWR22Rv1), and androgen‐independent prostate cancer cells (PC3).
RESULTS
Compared to PrEC and PZ‐HPV‐7 cells, all cancer cells exhibited elevated levels of detyrosinated and polyglutamylated α‐tubulin, that was paralleled by decreased protein levels of tubulin tyrosine ligase (TTL). In contrast, PrEC and PZ‐HPV‐7 cells expressed markedly higher levels of Δ2‐tubulin. Whereas α‐tubulin acetylation levels were generally equivalent in all the cell lines, PC3 cells did not display detectable levels of Ac‐tubulin.
CONCLUSION
These data may reveal novel biomarkers of prostate cancer and new therapeutic targets. Prostate 66: 954–965, 2006. © 2006 Wiley‐Liss, Inc.
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