Tumor-Suppressive Effect of Adenovirus-Mediated Inhibitor of Growth 4 Gene Transfer in Breast Carcinoma Cells In Vitro and In Vivo

2010 ◽  
Vol 25 (4) ◽  
pp. 427-437 ◽  
Author(s):  
Zhengyi Li ◽  
Yufeng Xie ◽  
Weihua Sheng ◽  
Jingcheng Miao ◽  
Jim Xiang ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Gene Transfer ◽  
Suppressive Effect ◽  
Carcinoma Cells ◽  
Breast Carcinoma Cells ◽  
Tumor Suppressive Effect

scholarly journals The conformational state of Tes regulates its zyxin-dependent recruitment to focal adhesions

2003 ◽  
Vol 161 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Boyan K. Garvalov ◽  
Theresa E. Higgins ◽  
James D. Sutherland ◽  
Markus Zettl ◽  
Niki Scaplehorn ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Focal Adhesions ◽  
Conformational State ◽  
Carcinoma Cells ◽  
Domain Organization ◽  
Breast Carcinoma Cells ◽  
Cell Extracts

The function of the human Tes protein, which has extensive similarity to zyxin in both sequence and domain organization, is currently unknown. We now show that Tes is a component of focal adhesions that, when expressed, negatively regulates proliferation of T47D breast carcinoma cells. Coimmunoprecipitations demonstrate that in vivo Tes is complexed with actin, Mena, and vasodilator-stimulated phosphoprotein (VASP). Interestingly, the isolated NH2-terminal half of Tes pulls out α-actinin and paxillin from cell extracts in addition to actin. The COOH-terminal half recruits zyxin as well as Mena and VASP from cell extracts. These differences suggest that the ability of Tes to associate with α-actinin, paxillin, and zyxin is dependent on the conformational state of the molecule. Consistent with this hypothesis, we demonstrate that the two halves of Tes interact with each other in vitro and in vivo. Using fibroblasts lacking Mena and VASP, we show that these proteins are not required to recruit Tes to focal adhesions. However, using RNAi ablation, we demonstrate that zyxin is required to recruit Tes, as well as Mena and VASP, but not vinculin or paxillin, to focal adhesions.

Imatinib-induced changes in gene expression and the metastatic potential of human breast carcinoma cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 1074-1074
Author(s):  
A. Lorico ◽  
F. Anzanello ◽  
G. Rappa
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Carcinoma Cells ◽  
Myelogenous Leukemia ◽  
Breast Carcinoma Cells

1074 Background: Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs). Since its advent for the successful treatment of chronic myelogenous leukemia in 2001, the clinical efficacy of imatinib has been investigated in many other human malignancies, including breast cancer. Based on recent reports that chemotherapy selects more invasive and metastasizing cells, we have hypothesized that exposure of breast cancer cells to imatinib could enhance their malignant behavior. Methods: MA-11 breast carcinoma cells, originating from bone marrow micrometastases, were exposed to imatinib in vitro for seven days. After four days of recovery in drug-free medium, biological properties and gene expression pattern were compared with those of the parental cell line. In a separate set of experiments, the effects of in vivo administration of imatinib to athymic nude (nu/nu) mice carrying MA-11 tumors were investigated. Results: In vitro, imatinib treatment increased the motility and invasiveness of the breast cancer cells, and induced over-expression of drug transporters and of a set of genes associated with aggressive and metastatic behavior (Table). In vivo, nu/nu mice subcutaneously implanted with MA-11 cells and treated with nine daily intraperitoneal doses of 60 mg/Kg imatinib developed with greater frequency distant organ metastases vs. control mice implanted with MA-11 and treated with the vehicle alone. Conclusions: Our data caution against the clinical use of imatinib in breast cancer; imatinib-selected breast cancer cells represent an important tool to investigate the pro-metastatic role of differentially expressed genes. [Table: see text] No significant financial relationships to disclose.

STX140 Is Efficacious In vitro and In vivo in Taxane-Resistant Breast Carcinoma Cells

2008 ◽  
Vol 14 (2) ◽  
pp. 597-606 ◽  
Author(s):  
S. P. Newman ◽  
P. A. Foster ◽  
C. Stengel ◽  
J. M. Day ◽  
Y. T. Ho ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Breast Carcinoma Cells

MRMT-1 rat breast carcinoma cells and models of bone metastases: Improvement of an in vitro system to mimic the in vivo condition

2013 ◽  
Vol 115 (1) ◽  
pp. 76-85 ◽  
Author(s):  
Francesca Salamanna ◽  
Lucia Martini ◽  
Stefania Pagani ◽  
Annapaola Parrilli ◽  
Gianluca Giavaresi ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Bone Metastases ◽  
Carcinoma Cells ◽  
In Vitro System ◽  
Breast Carcinoma Cells

scholarly journals MicroRNA-27a-5p inhibits proliferation, migration and invasion and promotes apoptosis of Wilms tumor cell by targeting PBOV1

2021 ◽  
Author(s):  
zhengtuan guo ◽  
qiang yv ◽  
chunlin miao ◽  
wenan ge ◽  
peng li
Keyword(s):  
Tumor Cells ◽  
Wilms Tumor ◽  
Suppressive Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tumor Tissues ◽  
And Function ◽  
Tumor Suppressive Effect

Wilms tumor is the most common type of renal tumor in children. MicroRNAs (miRNA) are small non-coding RNAs that play crucial regulatory roles in tumorigenesis. We aimed to study the expression profile and function of miR-27a-5p in Wilms tumor. MiR-27a-5p expression was downregulated in human Wilms tumor tissues. Functionally, overexpression of miR-27a-5p promoted cell apoptosis of Wilms tumor cells. Furthermore, upregulated miR-27a-5p delayed xenograft Wilms tumor tumorigenesis in vivo. Bioinformatics analysis predicted miR-27-5p directly targeted to the 3’-untranslated region (UTR) of PBOV1 and luciferase reporter assay confirmed the interaction between miR-27a-5p and PBOV1. The function of PBOV1 in Wilms tumor was evaluated in vitro and knockdown of PBOV1 dampened cell migration. In addition, overexpression of PBOV1 antagonized the tumor-suppressive effect of miR-27a-5p in Wilms tumor cells. Collectively, our findings reveal the regulatory axis of miR-27-5p/PBOV1 in Wilms tumor and miR-27a-5p might serve as a novel therapeutic target in Wilms tumor.

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