l-Cysteine/AgNO2 low molecular weight gelators: self-assembly and suppression of MCF-7 breast cancer cells

Soft Matter ◽  
2020 ◽  
Vol 16 (42) ◽  
pp. 9669-9673
Author(s):  
Dmitry V. Vishnevetskii ◽  
Arif R. Mekhtiev ◽  
Tatyana V. Perevozova ◽  
Dmitry V. Averkin ◽  
Alexandra I. Ivanova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Weight ◽  
Cancer Cells ◽  
Self Assembly ◽  
Breast Cancer Cells ◽  
Low Molecular Weight ◽  
Human Breast ◽  
Selective Toxicity ◽  
Low Molecular Weight Gelators ◽  
Mcf 7

We present a method for the preparation of a new hydrogel based on low molecular weight gelators that exhibits selective toxicity towards MCF-7 human breast cancer cells.

scholarly journals Overexpression of Cyclin E and its Low Molecular Weight Isoforms Cooperate with Loss of p53 in Promoting Oncogenic Properties of MCF-7 Breast Cancer Cells

2015 ◽  
Vol 16 (17) ◽  
pp. 7575-7582 ◽  
Author(s):  
Hamed Montazeri ◽  
Saeid Bouzari ◽  
Kayhan Azadmanesh ◽  
Seyed Nasser Ostad ◽  
Mohammad Hossein Ghahremani
Keyword(s):  
Breast Cancer ◽  
Molecular Weight ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cyclin E ◽  
Low Molecular Weight ◽  
Mcf 7

scholarly journals Novel TNBC-Targeted DOX-Arsonoliposomes

Proceedings ◽  
2020 ◽  
Vol 78 (1) ◽  
pp. 17
Author(s):  
Maria Mantzari ◽  
Foteini Gartziou ◽  
Eleni Lambrou ◽  
Spyridon Mourtas ◽  
Paraskevi Zagana ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Entrapment Efficiency ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Selective Toxicity ◽  
First Results

Arsonoliposomes (ARSL) constitute a particular class of liposomes that incorporate arsonolipids (ARS) into their membranes. ARSL realize selective toxicity to cancer cells; thus, they are an important tool in the treatment of cancer. Folic acid (FA) is widely used in targeted drug delivery due to its high affinity for the folate receptors that are overexpressed in cancer cell membranes. The aim of our studies was to develop novel triple-negative breast cancer (TNBC)-targeted ARSL by incorporating folic acid-conjugated polyethylene-glycol PEG-lipid (FA-PEG-lipid) into their membrane and loading them with anticancer drug doxorubicin (DOX). ARSL incorporating 0.1 mol% of FA-PEG-lipid were prepared and loaded with DOX, using the active loading protocol. They were characterized for their size distribution, zeta potential and drug entrapment efficiency (%). Their cytotoxic activity towards TNBC cell lines, particularly MDA-MB-231 (epithelial human breast cancer cells) and MCF7 (human breast cancer cells), was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT-assay. The first results demonstrated enhanced toxicity of this novel type of ARSL towards cancer cells, which is particularly interesting and deserves further exploitation.

scholarly journals Sphingosine Kinase Transmits Estrogen Signaling in Human Breast Cancer Cells

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7 ◽  
Cytoplasmic Signaling

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.

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