scholarly journals MAP Kinases and Prostate Cancer

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Gonzalo Rodríguez-Berriguete ◽  
Benito Fraile ◽  
Pilar Martínez-Onsurbe ◽  
Gabriel Olmedilla ◽  
Ricardo Paniagua ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Map Kinases ◽  
Tumor Promotion ◽  
Metastatic Potential ◽  
Mitogen Activated Protein Kinases ◽  
Signal Transducers ◽  
Cell Functions ◽  
Growing Body ◽  
Mitogen Activated Protein ◽  
Androgen Independent

The three major mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK are signal transducers involved in a broad range of cell functions including survival, apoptosis, and cell differentiation. Whereas JNK and p38 have been generally linked to cell death and tumor suppression, ERK plays a prominent role in cell survival and tumor promotion, in response to a broad range of stimuli such as cytokines, growth factors, ultraviolet radiation, hypoxia, or pharmacological compounds. However, there is a growing body of evidence supporting that JNK and p38 also contribute to the development of a number of malignances. In this paper we focus on the involvement of the MAPK pathways in prostate cancer, including the less-known ERK5 pathway, as pro- or antitumor mediators, through their effects on apoptosis, survival, metastatic potential, and androgen-independent growth.

Constitutive activation of the 41- and 43-kDa mitogen-activated protein (MAP) kinases in the progression of prostate cancer to an androgen-independent state

2005 ◽  
Vol 12 (10) ◽  
pp. 899-905 ◽  
Author(s):  
HIROYA OKA ◽  
YUJI CHATANI ◽  
MICHIAKI KOHNO ◽  
MUTSUSHI KAWAKITA ◽  
OSAMU OGAWA
Keyword(s):  
Prostate Cancer ◽  
Map Kinases ◽  
Independent State ◽  
Constitutive Activation ◽  
Protein Map ◽  
Mitogen Activated Protein ◽  
Androgen Independent

scholarly journals Clinical and Biomarker Correlates of Androgen-Independent, Locally Aggressive Prostate Cancer with Limited Metastatic Potential

2004 ◽  
Vol 10 (20) ◽  
pp. 6770-6778 ◽  
Author(s):  
Vasily J. Assikis ◽  
Kim-Anh Do ◽  
Sijin Wen ◽  
Xuemei Wang ◽  
Jeong Hee Cho-Vega ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Metastatic Potential ◽  
Aggressive Prostate Cancer ◽  
Androgen Independent

scholarly journals Mitogen-activated protein kinases mediate changes in gene expression, but not cytoskeletal organization associated with cardiac muscle cell hypertrophy.

1994 ◽  
Vol 126 (6) ◽  
pp. 1565-1572 ◽  
Author(s):  
J Thorburn ◽  
J A Frost ◽  
A Thorburn
Keyword(s):  
Protein Kinases ◽  
Map Kinases ◽  
Individual Cell ◽  
Treatment Results ◽  
Mitogen Activated Protein Kinases ◽  
Cytoskeletal Organization ◽  
Hypertrophic Response ◽  
Ras Protein ◽  
Cellular Hypertrophy ◽  
Mitogen Activated Protein

Shortly after birth, cardiac myocytes lose the ability to divide, and, in adult animals, heart muscle grows by a process of cellular hypertrophy where each individual cell gets larger. We have previously shown that activated Ras protein can induce markers of the hypertrophic phenotype, including atrial natriuretic factor (ANF) expression and organization of contractile proteins, and that Ras is at least partially required for the hypertrophic effect of phenylephrine. In the present study, we examine the requirement for the mitogen-activated protein kinases (MAP kinases) in the hypertrophic response induced by phenylephrine. We find that phenylephrine treatment results in the activation of the MAP kinases and that this activity is required for transactivation of the fos, ANF, and MLH promoters. However, inhibition of MAP kinases does not prevent phenylephrine-induced organization of actin. These results suggest that the signal transduction pathways leading to different hypertrophic responses diverge upstream of the MAP kinases but possibly downstream of Ras.

scholarly journals Genetic changes associated with the acquisition of androgen-independent growth, tumorigenicity and metastatic potential in a prostate cancer model

1997 ◽  
Vol 75 (2) ◽  
pp. 190-195 ◽  
Author(s):  
E-R Hyytinen ◽  
GN Thalmann ◽  
HE Zhau ◽  
R Karhu ◽  
O-P Kallioniemi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Metastatic Potential ◽  
Cancer Model ◽  
Genetic Changes ◽  
Androgen Independent ◽  
Prostate Cancer Model
Sign in / Sign up

Export Citation Format

Share Document