scholarly journals Silencing of Bcl-2 expression by small interfering RNA induces autophagic cell death in MCF-7 breast cancer cells

Autophagy ◽  
2008 ◽  
Vol 4 (5) ◽  
pp. 669-679 ◽  
Author(s):  
Ugur Akar ◽  
Arturo Chaves-Reyez ◽  
Magaly Barria ◽  
Ana Tari ◽  
Angela Sanguino ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Breast Cancer Cells ◽  
Autophagic Cell Death ◽  
Interfering Rna ◽  
Mcf 7

scholarly journals Unique Roles of p160 Coactivators for Regulation of Breast Cancer Cell Proliferation and Estrogen Receptor-α Transcriptional Activity

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1588-1596 ◽  
Author(s):  
Sudipan Karmakar ◽  
Estrella A. Foster ◽  
Carolyn L. Smith
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Breast Cancer Cells ◽  
Transcriptional Activity ◽  
Interfering Rna ◽  
Mcf 7

Each of the three members of the p160 steroid receptor coactivator (SRC) family of coactivators (SRC-1, SRC-2 and SRC-3) stimulates estrogen receptor (ER)-α function in trans-activation assays. Consequently, we sought to elucidate their contributions to the ER-regulated processes of cell proliferation, apoptosis, and the expression of ERα target genes in MCF-7 breast cancer cells. The small interfering RNA depletion of SRC-2 or SRC-3 but not SRC-1 inhibited growth of MCF-7 cells, and this was reflected in decreased cell cycle progression and increased apoptosis in SRC-2- or SRC-3-depleted cells as well as a reduction in ERα transcriptional activity measured on a synthetic reporter gene. However, only SRC-3 depletion blocked estradiol stimulated cell proliferation. Depletion of SRC-1 did not affect these events, and together this reveals functional differences between each of the three SRC family coactivators. Regulation of the endogenous ERα target gene, c-myc was not affected by depletion of any of the p160 coactivators although depletion of each of them decreased pS2 mRNA expression in estradiol-treated MCF-7 cells. Moreover, progesterone receptor and cyclin D1 gene expression were decreased in SRC-3 small interfering RNA-treated cells. Expression of mRNA and protein levels for the antiapoptotic gene, Bcl-2 was dependent on SRC-3 expression, whereas Bcl-2 protein but not mRNA expression also was sensitive to SRC-1 depletion. Together these data indicate that the closely related p160 coactivators are not functionally redundant in breast cancer cells because they play gene-specific roles in regulating mRNA and protein expression, and they therefore are likely to make unique contributions to breast tumorigenesis.

scholarly journals Gold Nanoparticles Increase PLK1-Specific Small Interfering RNA Transfection and Induce Apoptosis of Drug Resistance Breast Cancer Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Ying Tian ◽  
Yunlei Zhang ◽  
Jing Pan ◽  
Nan Lu ◽  
Shouju Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gold Nanoparticles ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Breast Cancer Cells ◽  
Low Cytotoxicity ◽  
Interfering Rna ◽  
Lipofectamine 2000 ◽  
Mcf 7

Drug resistance is a major barrier that limits the effectiveness of chemotherapies against breast cancer. Here, gold nanoparticles (GNPs) characterized by good dispersivity, high stability, low cytotoxicity, and simple synthesis were developed to deliver small interfering RNA (siRNA) against PLK1 (PLK1-siRNA) and overcome the drug resistance of breast cancer cells. Compared with the commonly used Lipofectamine 2000, GNPs showed higher PLK1-siRNA delivery efficiency and resulted in the remarkable gene silencing ofPLK1in drug resistance breast cancer cells MCF-7/MDR1 with low cytotoxicityin vitro. Moreover, delivery of PLK1-siRNA by GNPs could cause 14.23% apoptosis of MCF-7/MDR1 cells, which was apparently higher than 11.01% apoptosis conducted by Lipofectamine 2000. In addition, GNPs showed strong X-ray attenuation coefficient, indicating the potential theranostic application of this system. Therefore, this study disclosed an important step in the use of GNPs as transfection vector of siRNA that will be of great benefit to gene therapy against drug resistant cancer.

scholarly journals Molecular Mechanism of SAHA on Regulation of Autophagic Cell Death in Tamoxifen-Resistant MCF-7 Breast Cancer Cells

2012 ◽  
Vol 9 (10) ◽  
pp. 881-893 ◽  
Author(s):  
Young Ju Lee ◽  
A Jin Won ◽  
Jaewon Lee ◽  
Jee H. Jung ◽  
Sungpil Yoon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Breast Cancer Cells ◽  
Autophagic Cell Death ◽  
Tamoxifen Resistant ◽  
Mcf 7

scholarly journals Doxorubicin resistance mediated by cytoplasmic macrophage colony-stimulating factor is associated with switch from apoptosis to autophagic cell death in MCF-7 breast cancer cells

2016 ◽  
Vol 241 (18) ◽  
pp. 2086-2093 ◽  
Author(s):  
Mengxia Zhang ◽  
Hailiang Zhang ◽  
Fan Tang ◽  
Yuhua Wang ◽  
Zhongcheng Mo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Colony Stimulating Factor ◽  
Doxorubicin Resistance ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Mcf 7

Macrophage colony-stimulating factor is a vital factor in maintaining the biological function of monocyte–macrophage lineage. It is expressed in many tumor tissues and cancer cells. Recent findings indicate that macrophage colony-stimulating factor might contribute to chemoresistance, but the precise mechanisms are unclear. This study was to explore the effect of macrophage colony-stimulating factor on doxorubicin resistance in MCF-7 breast cancer cells and the possible mechanism. In the study, the human breast cancer cells, MCF-7, were transfected with macrophage colony-stimulating factor. We document that cytoplasmic macrophage colony-stimulating factor induces doxorubicin resistance and inhibits apoptosis in MCF-7 cells. Further studies demonstrated that cytoplasmic macrophage colony-stimulating factor-mediated apoptosis inhibition was dependent on the activation of PI3K/Akt/Survivin pathway. More importantly, we found that macrophage colony-stimulating factor-induced autophagic cell death in doxorubicin-treated MCF-7 cells. Taken together, we show for the first time that macrophage colony-stimulating factor-induced doxorubicin resistance is associated with the changes in cell death response with defective apoptosis and promotion of autophagic cell death.

Methotrexate induced cell death mechanisms in MCF-7 adenocarcinoma breast cancer cells: Enhanced cytotoxicity following dff45-siRNA pre-treatment

Synergy ◽  
2018 ◽  
Vol 7 ◽  
pp. 10-16
Author(s):  
Fatemeh Kiani ◽  
Negin Rasouli ◽  
Tahereh Kashkoolinejad ◽  
Shahrokh Safarian ◽  
Seyed Jalal Zargar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Pre Treatment ◽  
Cell Death Mechanisms ◽  
Mcf 7
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