Potent anti‐inflammatory Terminalia chebula fruit showed in vitro anticancer activity on lung and breast carcinoma cells through the regulation of Bax/Bcl‐2 and caspase‐cascade pathways

2020 ◽  
Vol 44 (12) ◽  
Author(s):  
Anil Khushalrao Shendge ◽  
Rhitajit Sarkar ◽  
Nripendranath Mandal
Keyword(s):  
Breast Carcinoma ◽  
Anticancer Activity ◽  
Carcinoma Cells ◽  
Terminalia Chebula ◽  
Breast Carcinoma Cells ◽  
Caspase Cascade ◽  
Anti Inflammatory

scholarly journals In vitro elucidation of the role of pericellular matrix in metastatic extravasation and invasion of breast carcinoma cells

2018 ◽  
Vol 10 (4) ◽  
pp. 242-252 ◽  
Author(s):  
Marie-Elena Brett ◽  
Heather E. Bomberger ◽  
Geneva R. Doak ◽  
Matthew A. Price ◽  
James B. McCarthy ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Malignant Progression ◽  
Pericellular Matrix ◽  
Breast Carcinoma Cells

The hyaluronan-rich pericellular matrix is an important feature of malignant progression in breast carcinoma.

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.

scholarly journals Role of miR-100-5p and CDC25A in breast carcinoma cells

PeerJ ◽  
2022 ◽  
Vol 9 ◽  
pp. e12263
Author(s):  
Xiaoping Li ◽  
Yanli Ren ◽  
Donghong Liu ◽  
Xi Yu ◽  
Keda Chen
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Breast Carcinoma Cells ◽  
Cell Functions ◽  
Relationship Of

Objective To inquiry about mechanism of miR-100-5p/CDC25A axis in breast carcinoma (BC), thus offering a new direction for BC targeted treatment. Methods qRT-PCR was employed to explore miR-100-5p and CDC25A mRNA levels. Western blot was employed for detecting protein expression of CDC25A. Targeting relationship of miR-100-5p and CDC25A was verified by dual-luciferase assay. In vitro experiments were used for assessment of cell functions. Results In BC tissue and cells, miR-100-5p was significantly lowly expressed (P < 0.05) while CDC25A was highly expressed. Besides, miR-100-5p downregulated CDC25A level. miR-100-5p had a marked influence on the prognosis of patients. The forced miR-100-5p expression hindered BC cell proliferation, migration and invasion, and facilitated cell apoptosis. Upregulated miR-100-5p weakened promotion of CDC25A on BC cell growth. Conclusion Together, these findings unveiled that CDC25A may be a key target of miR-100-5p that mediated progression of BC cells. Hence, miR-100-5p overexpression or CDC25A suppression may contribute to BC diagnosis.

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