scholarly journals Ectopic Synthesis of Coagulation Factor VII in Breast Cancer Cells: Mechanisms, Functional Correlates, and Potential for a New Therapeutic Target

10.5772/21757 ◽  
2011 ◽  
Author(s):  
Shiro Koizume ◽  
Yohei Miyagi
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Coagulation Factor Vii

scholarly journals Spot 14: A Marker of Aggressive Breast Cancer and a Potential Therapeutic Target

Endocrinology ◽  
2006 ◽  
Vol 147 (9) ◽  
pp. 4048-4055 ◽  
Author(s):  
William B. Kinlaw ◽  
Jennifer L. Quinn ◽  
Wendy A. Wells ◽  
Christopher Roser-Jones ◽  
Joel T. Moncur
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Milk Fat ◽  
Breast Cancer Cells ◽  
De Novo ◽  
Lipid Synthesis ◽  
Breast Cancers ◽  
Spot 14 ◽  
Aggressive Breast Cancer

Spot 14 (S14) is a nuclear protein that communicates the status of dietary fuels and fuel-related hormones to genes required for long-chain fatty acid synthesis. In mammary gland, S14 is important for both epithelial proliferation and milk fat production. The S14 gene is amplified in some breast cancers and is strongly expressed in most. High expression of S14 in primary invasive breast cancer is conspicuously predictive of recurrence. S14 mediates the induction of lipogenesis by progestin in breast cancer cells and accelerates their growth. Conversely, S14 knockdown impairs de novo lipid synthesis and causes apoptosis. We found that breast cancer cells do not express lipoprotein lipase (LPL) and hypothesize that they do not have access to circulating lipids unless the local environment supplies it. This may explain why primary breast cancers with low S14 do not survive transit from the LPL-rich mammary fat pad to areas devoid of LPL, such as lymph nodes, and thus do not appear as distant metastases. Thus, S14 is a marker for aggressive breast cancer and a potential target as well. Future effort will center on validation of S14 as a therapeutic target and producing antagonists of its action.

scholarly journals Fatty acid synthase phosphorylation: a novel therapeutic target in HER2-overexpressing breast cancer cells

2010 ◽  
Vol 12 (6) ◽  
Author(s):  
Quanri Jin ◽  
Linda X Yuan ◽  
Delphine Boulbes ◽  
Jong Min Baek ◽  
Ying Nai Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Fatty Acid Synthase ◽  
Novel Therapeutic

scholarly journals Connexin43 pseudogene in breast cancer cells offers a novel therapeutic target

2009 ◽  
Vol 8 (4) ◽  
pp. 786-793 ◽  
Author(s):  
Andrew Bier ◽  
Irene Oviedo-Landaverde ◽  
Jing Zhao ◽  
Yael Mamane ◽  
Mustapha Kandouz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Novel Therapeutic

scholarly journals ”BIK/NBK Gene Expression as a Possible Marker of Circulating Breast Cancer Cells in Blood“

2011 ◽  
Vol 4 (1) ◽  
pp. 8-14
Author(s):  
E. Lopez-Munoz ◽  
N. Garcia-Hernandez ◽  
R. I. Penaloza-Espinosa ◽  
M. E. Gomez-Del Toro ◽  
G. Zarco-Espinosa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Mrna Gene

The detection of circulating breast cancer cells in blood could be of special interest as an indicator of diagnosis and prognosis, and for the selection of treatment. In a previous report, our research group determined gene expression profiles in samples of breast cancer tissue, identifying over-expression of the BIK/NBK mRNA gene in 90% of the analyzed samples. In this paper, we analyze the BIK/NBK gene expression as a possible biomarker of circulating breast cancer cells in blood. We demonstrate that the BIK/NBK gene expression is not a significant biomarker in the detection of circulating breast cancer cells in the blood of women with breast cancer. Several studies have evaluated the regulation of apoptosis by estrogens in breast cancer cells, demonstrating the importance of BIK/NBK protein, in estrogen-regulated breast cancer cell apoptosis, which suggests that the regulation of its expression may be an important therapeutic target or strategy in the management of cancer, and, although we did not find statistically significant differences among the patient groups to demonstrate that BIK/NBK gene expression is a biomarker of circulating breast cancer cells in blood, we consider it necessary to continue the study of this gene in breast cancer tissue and its role in the development and progression of breast cancer, its prognostic value, and its potential use as therapeutic target.

scholarly journals hsa-miR-33-5p as a Therapeutic Target Promotes Apoptosis of Breast Cancer Cells via Selenoprotein T

2021 ◽  
Vol 8 ◽  
Author(s):  
Wei Zhuang ◽  
Jianhui Liu ◽  
Wenjin Li
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Selenoprotein T ◽  
Cancer Tissues ◽  
Mcf 7

Objective: Increasing evidence suggests that microRNA (miRNA) participates in regulating tumor cell apoptosis. We aimed to observe the effect of hsa-miR-33-5p on the apoptosis of breast cancer cells and to explore its regulatory relationship with selenoprotein T (SelT).Methods: RT-qPCR was used to examine the expression of hsa-miR-33-5p and SelT both in breast cancer tissues and cells. MCF-7 and MDA-MB-231 cells were transfected with hsa-miR-33-5p mimics or si-SelT. Then, a flow cytometry assay was carried out to examine the apoptosis of cells. Furthermore, SelT and apoptosis-related proteins including caspase-3, caspase-8, caspase-9, Bax, and Bcl-2 were detected via RT-qPCR and western blot. A luciferase reporter assay was utilized for assessing whether SelT was targeted by hsa-miR-33-5p.Results: Downregulated hsa-miR-33-5p was found both in breast cancer tissues and cells. After its overexpression, MCF-7 cell apoptosis was significantly promoted. Furthermore, our data showed that miR-33-5p elevated apoptosis-related protein expression in MCF-7 cells. Contrary to hsa-miR-33-5p, SelT was upregulated both in breast cancer tissues and cells. SelT expression was significantly inhibited by hsa-miR-33-5p overexpression. The luciferase reporter assay confirmed that SelT was a direct target of hsa-miR-33-5p. SelT overexpression could ameliorate the increase in apoptosis induced by hsa-miR-33-5p mimics.Conclusion: Our findings revealed that hsa-miR-33-5p, as a potential therapeutic target, could accelerate breast cancer cell apoptosis.

scholarly journals Bcl-3 promotes multi-modal tumour cell migration via NF-κB1 mediated regulation of Cdc42

2020 ◽  
Vol 41 (10) ◽  
pp. 1432-1443 ◽  
Author(s):  
Daniel J Turnham ◽  
William W Yang ◽  
Julia Davies ◽  
Athina Varnava ◽  
Anne J Ridley ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cell Motility ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Metastatic Tumour ◽  
Tumour Burden

Abstract A key challenge in the implementation of anti-metastatics as cancer therapies is the multi-modal nature of cell migration, which allows tumour cells to evade the targeted inhibition of specific cell motility pathways. The nuclear factor-kappaB (NF-κB) co-factor B-cell lymphoma 3 (Bcl-3) has been implicated in breast cancer cell migration and metastasis, yet it remains to be determined exactly which cell motility pathways are controlled by Bcl-3 and whether migrating tumour cells are able to evade Bcl-3 intervention. Addressing these questions and the mechanism underpinning Bcl-3’s role in this process would help determine its potential as a therapeutic target. Here we identify Bcl-3 as an upstream regulator of the two principal forms of breast cancer cell motility, involving collective and single-cell migration. This was found to be mediated by the master regulator Cdc42 through binding of the NF-κB transcription factor p50 to the Cdc42 promoter. Notably, Bcl-3 depletion inhibited both stable and transitory motility phenotypes in breast cancer cells with no evidence of migratory adaptation. Overexpression of Bcl-3 enhanced migration and increased metastatic tumour burden of breast cancer cells in vivo, whereas overexpression of a mutant Bcl-3 protein, which is unable to bind p50, suppressed cell migration and metastatic tumour burden suggesting that disruption of Bcl-3/NF-κB complexes is sufficient to inhibit metastasis. These findings identify a novel role for Bcl-3 in intrinsic and adaptive multi-modal cell migration mediated by its direct regulation of the Rho GTPase Cdc42 and identify the upstream Bcl-3:p50 transcription complex as a potential therapeutic target for metastatic disease.

An HDAC8-Selective Fluorescent Probe for Imaging in Living Tumor Cell Lines and Tissue Slices

2021 ◽  
Author(s):  
Yinyu Yan ◽  
chaoqun huang ◽  
Yi Shu ◽  
Hongmei Wen ◽  
Chenxiao Shan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Neuroblastoma Cells ◽  
Tumor Cell Lines ◽  
Tissue Slices ◽  
Histone Deacetylase 8

The histone deacetylase 8 (HDAC8) used as therapeutic target for many cancers such as highly expressed in neuroblastoma cells and breast cancer cells. HDAC8- selective fluorescent probes needed to be...

Abstract LB-180: Notch-1: A therapeutic target for breast cancer stem cells and breast cancer cells

2012 ◽  
Author(s):  
Suman Suman ◽  
Trinath P. Das ◽  
Vittal Kurisetty ◽  
Thippeswamy Gulappa ◽  
Aditi Shirish Vadodkar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Breast Cancer Stem Cells ◽  
Notch 1
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