JNK-related papers

Mesothelin Enhances Invasion of Ovarian Cancer by Inducing

Postby kinoob » Fri Oct 21, 2011 9:50 am

Mesothelin enhances invasion of ovarian cancer by inducing MMP-7 through MAPK/ERK and JNK pathways

Biochem J. 2012 Mar 1;442(2):293-302
Chang MC, Chen CA, Chen PJ, Chiang YC, Chen YL, Mao TL, Lin HW, Lin Chiang WH, Cheng WF
Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan

Abstract

Ovarian cancer has one of the highest mortalities in malignancies in women, but little is known of its tumour progression properties and there is still no effective molecule that can monitor its growth or therapeutic responses. MSLN (mesothelin), a secreted protein that is overexpressed in ovarian cancer tissues with a poor clinical outcome, has been previously identified to activate PI3K (phosphoinositide 3-kinase)/Akt signalling and inhibit paclitaxel-induced apoptosis. The present study investigates the correlation between MSLN and MMP (matrix metalloproteinase)-7 in the progression of ovarian cancer, and the mechanism of MSLN in enhancing ovarian cancer invasion. The expression of MSLN correlated well with MMP-7 expression in human ovarian cancer tissues. Overexpressing MSLN or ovarian cancer cells treated with MSLN showed enhanced migration and invasion of cancer cells through the induction of MMP-7. MSLN regulated the expression of MMP-7 through the ERK (extracellular-signal-regulated kinase) 1/2, Akt and JNK (c-Jun N-terminal kinase) pathways. The expression of MMP-7 and the migrating ability of MSLN-treated ovarian cancer cells were suppressed by ERK1/2- or JNK-specific inhibitors, or a decoy AP-1 (activator protein 1) oligonucleotide in in vitro experiments, whereas in vivo animal experiments also demonstrated that mice treated with MAPK (mitogen-activated protein kinase)/ERK- or JNK-specific inhibitors could decrease intratumour MMP-7 expression, delay tumour growth and extend the survival of the mice. In conclusion, MSLN enhances ovarian cancer invasion by MMP-7 expression through the MAPK/ERK and JNK signal transduction pathways. Blocking the MSLN-related pathway could be a potential strategy for inhibiting the growth of ovarian cancer.

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed/21999204
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JNK-related papers

Postby CellSigNet » Fri Jun 01, 2012 3:04 am

Put all JNK cascade related papers here, please

If you can't access these articles, please let me know.
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Re: JNK-related papers

Postby CellSigNet » Fri Jun 01, 2012 3:11 am

JNK-induced apoptosis, compensatory growth, and cancer stem cells

Cancer Res. 2012 Jan 15;72(2):379-86
Chen F
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan 48201, USA

Abstract

Overwhelming are a set of key stress-responsive kinases that mediate cell apoptosis, which is an important process for tumor suppression. However, JNKs have also been implicated in the malignant transformation and tumorigenesis of cells. This review attempts to reconcile these 2 contradictory functions of JNKs with recent discoveries on the role of JNKs in compensatory growth of neighboring cells and stem cells, which may provide new mechanistic understanding about the role of JNKs in the regulation of cancer stem cells and the pathogenesis of cancers.

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed/22253282
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Re: JNK-related papers

Postby CellSigNet » Fri Jun 01, 2012 3:14 am

Diverse Roles of JNK and MKK Pathways in the Brain

J Signal Transduct. 2012;2012:459265. Epub 2012 Feb 8
Yamasaki T, Kawasaki H, Nishina H
Department of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan

Abstract

The c-Jun NH(2)-terminal protein kinase (JNK) plays important roles in a broad range of physiological processes. JNK is controlled by two upstream regulators, mitogen-activated protein kinase kinase (MKK) 4 and MKK7, which are activated by various MAPKKKs. Studies employing knockout mice have demonstrated that the JNK signaling pathway is involved in diverse phenomena in the brain, regulating brain development and maintenance as well as animal metabolism and behavior. Furthermore, examination of single or combined knockout mice of Jnk1, Jnk2, and Jnk3 has revealed both functional differences and redundancy among JNK1, JNK2, and JNK3. Phenotypic differences between knockouts of MKK4 and MKK7 have also been observed, suggesting that the JNK signaling pathway in the brain has a complex nature and is intricately regulated. This paper summarizes the functional properties of the major JNK signaling components in the developing and adult brain.

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed/22496975
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Re: JNK-related papers

Postby CellSigNet » Fri Jun 01, 2012 3:17 am

c-Jun, at the crossroad of the signaling network

Protein Cell. 2011 Nov;2(11):889-98
Meng Q, Xia Y
Department of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, OH 45267, USA

Abstract

c-Jun, the most extensively studied protein of the activator protein-1 (AP-1) complex, is involved in numerous cell activities, such as proliferation, apoptosis, survival, tumorigenesis and tissue morphogenesis. Earlier studies focused on the structure and function have led to the identification of c-Jun as a basic leucine zipper (bZIP) transcription factor that acts as homo- or heterodimer, binding to DNA and regulating gene transcription. Later on, it was shown that extracellular signals can induce post-translational modifications of c-Jun, resulting in altered transcriptional activity and target gene expression. More recent work has uncovered multiple layers of a complex regulatory scheme in which c-Jun is able to crosstalk, amplify and integrate different signals for tissue development and disease. One example of such scheme is the autocrine amplification loop, in which signal-induced AP-1 activates the c-Jun gene promoter, while increased c-Jun expression feedbacks to potentiate AP-1 activity. Another example of such scheme, based on recent characterization of gene knockout mice, is that c-Jun integrates signals of several developmental pathways, including EGFR-ERK, EGFR-RhoA-ROCK, and activin B-MAP3K1-JNK for embryonic eyelid closure. After more than two decades of extensive research, c-Jun remains at the center stage of a molecular network with mysterious functional properties, some of which are yet to be discovered. In this article, we will provide a brief historical overview of studies on c-Jun regulation and function, and use eyelid development as an example to illustrate the complexity of c-Jun crosstalking with signaling pathways.

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed/22180088
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