Faculty Opinions recommendation of The cochaperone p23 differentially regulates estrogen receptor target genes and promotes tumor cell adhesion and invasion.

2006 ◽  
Author(s):  
Paul Webb
Keyword(s):  
Estrogen Receptor ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Target Genes ◽  
Tumor Cell Adhesion ◽  
Adhesion And Invasion

scholarly journals The Cochaperone p23 Differentially Regulates Estrogen Receptor Target Genes and Promotes Tumor Cell Adhesion and Invasion

2006 ◽  
Vol 26 (14) ◽  
pp. 5205-5213 ◽  
Author(s):  
Ellinor Oxelmark ◽  
Jennifer M. Roth ◽  
Peter C. Brooks ◽  
Steven E. Braunstein ◽  
Robert J. Schneider ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Target Genes ◽  
Regulatory Element ◽  
Gene Activation ◽  
Tumor Development ◽  
Tumor Cell Adhesion ◽  
Cellular Processes ◽  
Estrogen Response ◽  
Adhesion And Invasion

ABSTRACT The cochaperone p23 plays an important role in estrogen receptor alpha (ER) signal transduction. In this study, we investigated how p23 regulates ER target gene activation and affects tumor growth and progression. Remarkably, we found that changes in the expression of p23 differentially affected the activation of ER target genes in a manner dependent upon the type of DNA regulatory element. p23 overexpression enhanced the expression of the ER target genes cathepsin D and pS2, which are regulated by direct DNA binding of ER to estrogen response elements (ERE). In contrast, the expression of other target genes, including c-Myc, cyclin D1, and E2F1, to which ER is recruited indirectly through its interaction with other transcription factors remains unaffected by changes in p23 levels. The p23-induced expression of pS2 is associated with enhanced recruitment of ER to the ERE in the promoter, whereas ER recruitment to the ERE-less c-Myc promoter does not respond to p23. Intriguingly, p23-overexpressing MCF-7 cells exhibit increased adhesion and invasion in the presence of fibronectin. Our findings demonstrate that p23 differentially regulates ER target genes and is involved in the control of distinct cellular processes in breast tumor development, thus revealing novel functions of this cochaperone.

PI3Kγ activation by CXCL12 regulates tumor cell adhesion and invasion

2009 ◽  
Vol 388 (2) ◽  
pp. 199-204 ◽  
Author(s):  
María Monterrubio ◽  
Mario Mellado ◽  
Ana C. Carrera ◽  
José Miguel Rodríguez-Frade
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion ◽  
Adhesion And Invasion

scholarly journals Endotoxin/Lipopolysaccharide Activates NF-κB and Enhances Tumor Cell Adhesion and Invasion Through a β1Integrin-Dependent Mechanism

2003 ◽  
Vol 170 (2) ◽  
pp. 795-804 ◽  
Author(s):  
Jiang Huai Wang ◽  
Brian J. Manning ◽  
Qiong Di Wu ◽  
Siobhan Blankson ◽  
D. Bouchier-Hayes ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion ◽  
Adhesion And Invasion ◽  
Dependent Mechanism

scholarly journals Sortilin is associated with breast cancer aggressiveness and contributes to tumor cell adhesion and invasion

Oncotarget ◽  
2015 ◽  
Vol 6 (12) ◽  
pp. 10473-10486 ◽  
Author(s):  
Séverine Roselli ◽  
Jay Pundavela ◽  
Yohann Demont ◽  
Sam Faulkner ◽  
Sheridan Keene ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion ◽  
Cancer Aggressiveness ◽  
Adhesion And Invasion

Matrix Metalloproteinase-8 Functions as a Metastasis Suppressor through Modulation of Tumor Cell Adhesion and Invasion

2008 ◽  
Vol 68 (8) ◽  
pp. 2755-2763 ◽  
Author(s):  
A. Gutierrez-Fernandez ◽  
A. Fueyo ◽  
A. R. Folgueras ◽  
C. Garabaya ◽  
C. J. Pennington ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Matrix Metalloproteinase ◽  
Tumor Cell ◽  
Metastasis Suppressor ◽  
Tumor Cell Adhesion ◽  
Adhesion And Invasion

Platelet and Shear Rate Promote Tumor Cell Adhesion to Human Endothelial Extracellular Matrix - Absence of a Role for Platelet Cyclooxygenase

1989 ◽  
Vol 61 (03) ◽  
pp. 485-489 ◽  
Author(s):  
Eva Bastida ◽  
Lourdes Almirall ◽  
Antonio Ordinas
Keyword(s):  
Cell Adhesion ◽  
Shear Rate ◽  
Tumor Cell ◽  
Umbilical Vein ◽  
Blood Platelets ◽  
Flow Conditions ◽  
Tumor Cell Adhesion ◽  
Rate Dependent ◽  
Static Conditions

SummaryBlood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 × 105 pl/μl in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.

Sign in / Sign up

Export Citation Format

Share Document