Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity

Chaehwa Park; Inkyoung Lee; Jun Ho Jang; Won Ki Kang

doi:10.1016/j.febslet.2007.07.007

Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity

Chaehwa Park, Inkyoung Lee, Jun Ho Jang, Won Ki Kang

Sungkyunkwan University

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

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.

Original language	English
Pages (from-to)	3800-3804
Number of pages	5
Journal	FEBS Letters
Volume	581
Issue number	20
DOIs	https://doi.org/10.1016/j.febslet.2007.07.007
State	Published - 7 Aug 2007
Externally published	Yes

Keywords

Erk
Phosphatase
RhoA
Senescence

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2007.07.007

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title = "Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity",

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.",

keywords = "Erk, Phosphatase, RhoA, Senescence",

author = "Chaehwa Park and Inkyoung Lee and Jang, \{Jun Ho\} and Kang, \{Won Ki\}",

year = "2007",

month = aug,

day = "7",

doi = "10.1016/j.febslet.2007.07.007",

language = "English",

volume = "581",

pages = "3800--3804",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "John Wiley and Sons Inc",

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TY - JOUR

T1 - Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity

AU - Park, Chaehwa

AU - Lee, Inkyoung

AU - Jang, Jun Ho

AU - Kang, Won Ki

PY - 2007/8/7

Y1 - 2007/8/7

N2 - 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.

AB - 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.

KW - Erk

KW - Phosphatase

KW - RhoA

KW - Senescence

UR - https://www.scopus.com/pages/publications/34547101470

U2 - 10.1016/j.febslet.2007.07.007

DO - 10.1016/j.febslet.2007.07.007

M3 - Article

C2 - 17658517

AN - SCOPUS:34547101470

SN - 0014-5793

VL - 581

SP - 3800

EP - 3804

JO - FEBS Letters

JF - FEBS Letters

IS - 20

ER -

Inhibitory role of RhoA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity

Abstract

Keywords

UN SDGs

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