scholarly journals Anti-proliferative and gene expression actions of resveratrol in breast cancer cells in vitro

Oncotarget ◽  
2014 ◽  
Vol 5 (24) ◽  
pp. 12891-12907 ◽  
Author(s):  
Yu-Tang Chin ◽  
Meng-Ti Hsieh ◽  
Sheng-Huei Yang ◽  
Po-Wei Tsai ◽  
Shwu-Huey Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Protein arginine methyltransferase 6-dependent gene expression and splicing: association with breast cancer outcomes

2012 ◽  
Vol 19 (4) ◽  
pp. 509-526 ◽  
Author(s):  
Dennis H Dowhan ◽  
Matthew J Harrison ◽  
Natalie A Eriksson ◽  
Peter Bailey ◽  
Michael A Pearen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Alternative Splicing ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Gene Expression Signature ◽  
Human Breast ◽  
Arginine Methyltransferase ◽  
Breast Tumours

Protein arginine methyltransferase-6 (PRMT6) regulates steroid-dependent transcription and alternative splicing and is implicated in endocrine system development and function, cell death, cell cycle, gene expression and cancer. Despite its role in these processes, little is known about its function and cellular targets in breast cancer. To identify novel gene targets regulated by PRMT6 in breast cancer cells, we used a combination of small interfering RNA and exon-specific microarray profilingin vitrocoupled toin vivovalidation in normal breast and primary human breast tumours. This approach, which allows the examination of genome-wide changes in individual exon usage and total transcript levels, demonstrated thatPRMT6knockdown significantly affected i) the transcription of 159 genes and ii) alternate splicing of 449 genes. ThePRMT6-dependent transcriptional and alternative splicing targets identifiedin vitrowere validated in human breast tumours. Using the list of genes differentially expressed between normal andPRMT6knockdown cells, we generated aPRMT6-dependent gene expression signature that provides an indication of PRMT6 dysfunction in breast cancer cells. Interrogation of several well-studied breast cancer microarray expression datasets with thePRMT6gene expression signature demonstrated that PRMT6 dysfunction is associated with better overall relapse-free and distant metastasis-free survival in the oestrogen receptor (ER (ESR1)) breast cancer subgroup. These results suggest that dysregulation ofPRMT6-dependent transcription and alternative splicing may be involved in breast cancer pathophysiology and the molecular consequences identifying a unique and informative biomarker profile.

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 Homeopathic Medicines Do Not Alter Growth and Gene Expression in Prostate and Breast Cancer Cells In Vitro

2006 ◽  
Vol 5 (4) ◽  
pp. 356-361 ◽  
Author(s):  
Rajesh L. Thangapazham ◽  
Jaya P. Gaddipati ◽  
N. V. Rajeshkumar ◽  
Anuj Sharma ◽  
Anoop K. Singh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Enhanced Gene Expression in Breast Cancer Cells in Vitro and Tumors in Vivo

2002 ◽  
Vol 6 (6) ◽  
pp. 783-792 ◽  
Author(s):  
Huanzhang Lu ◽  
Yufeng Zhang ◽  
David D. Roberts ◽  
C.Kent Osborne ◽  
Nancy Smyth Templeton
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells

The effects of RKIP gene expression on the biological characteristics of human triple-negative breast cancer cells in vitro

Tumor Biology ◽  
2012 ◽  
Vol 33 (4) ◽  
pp. 1159-1167 ◽  
Author(s):  
Chunfang Hao ◽  
Sen Wei ◽  
Zhongsheng Tong ◽  
Shufen Li ◽  
Yehui Shi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Biological Characteristics

scholarly journals Prolactin and oestrogen synergistically regulate gene expression and proliferation of breast cancer cells

2010 ◽  
Vol 17 (3) ◽  
pp. 809-822 ◽  
Author(s):  
Louise Maymann Rasmussen ◽  
Klaus Stensgaard Frederiksen ◽  
Nanni Din ◽  
Elisabeth Galsgaard ◽  
Leif Christensen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Regulation Of Gene Expression ◽  
Pituitary Hormone

The pituitary hormone prolactin (PRL) plays an important role in mammary gland development. It was also suggested to contribute to breast cancer progression. In vivo data strongly supported a crucial role of PRL in promoting tumour growth; however, PRL demonstrated only a weak, if any, pro-proliferative effect on cancer cells in vitro. Several recent studies indicated that PRL action in vivo may be influenced by the hormonal milieu, e.g. other growth factors such as 17β-oestradiol (E2). Here, we explored the potential interplay between PRL and E2 in regulation of gene expression and cell growth. PRL alone induced either a weak or no proliferative response of T47D and BT-483 cells respectively, while it drastically enhanced cell proliferation in E2-stimulated cultures. Affymetrix microarray analysis revealed 12 genes to be regulated by E2, while 57 genes were regulated by PRL in T47D cells. Most of the PRL-regulated genes (42/57) were not previously described as PRL target genes, e.g. WT1 and IER3. One hundred and five genes were found to be regulated upon PRL/E2 co-treatment: highest up-regulation was found for EGR3, RUNX2, EGR1, MAFF, GLIPR1, IER3, SOCS3, WT1 and AREG. PRL and E2 synergised to regulate EGR3, while multiple genes were regulated additively. These data show a novel interplay between PRL and E2 to modulate gene regulation in breast cancer cells.

Urtica dioica Extract Inhibits Proliferation and Induces Apoptosis and Related Gene Expression of Breast Cancer Cells In Vitro and In Vivo

2017 ◽  
Vol 17 (6) ◽  
pp. 463-470 ◽  
Author(s):  
Ali Mohammadi ◽  
Behzad Mansoori ◽  
Pooneh Chokhachi Baradaran ◽  
Vahid Khaze ◽  
Mahyar Aghapour ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Urtica Dioica ◽  
Related Gene
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