Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity |
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Authors: | Park Chaehwa Lee Inkyoung Jang Jun Ho Kang Won Ki |
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Institution: | Cancer Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Kangnam-gu, Seoul 135-710, Republic of Korea. cpark@smc.samsung.co.kr |
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Abstract: | Recently, negative effects of phosphatase in tumorigenesis and metastasis have been suggested in various tumor types. In this study, we showed that RhoA activation modulated phosphatase during senescence-like arrest in human prostate cancer cells. Under senescence-inducing condition, decreased Erk phosphorylation was detected in caRhoA-transfected cells and inactivation of Erk, but not p38, prevented doxorubicin-induced cell senescence. Cells were induced to senescence by inhibition of phosphatase activity (VHR, MKP3, or PP2A) without additional cellular stress. Of interest, caRhoA prevented doxorubicin-induced decrease of phosphatase. Thus, we postulate that RhoA signaling may protect cells against cellular senescence by maintaining phosphatase activity and Erk dephosphorylation. |
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Keywords: | RhoA Erk Phosphatase Senescence |
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