scholarly journals Preparation of chitosan-Epigallocatechin-3-O-gallate nanoparticles and their inhibitory effect on the growth of breast cancer cells

2018 ◽  
Vol 11 (04) ◽  
pp. 1850018 ◽  
Author(s):  
Yingyi Liu ◽  
Siyi Hu ◽  
Yueshu Feng ◽  
Peng Zou ◽  
Yue Wang ◽  
...  

In this paper, we prepared the nanoparticle drug carrier system between nanoparticles — chitosan and Epigallocatechin-3-O-gallate (EGCG) for breast cancer cell inhibiting application. For this drug carrier system, chitosan acts as a carrier and EGCG as a drug. Which were systematically characterized and thoroughly evaluated in terms of their inhibition rate and biocompatibility. We also did a cell scratch test and the result indicated that the chitosan-EGCG nanoparticles have inhibitory effect on the growth of breast cancer cells. The inhibition rate could reach up to 21.91%. This work revealed that the modification of nanoparticles paved a way for specific biomedical applications.

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2116
Author(s):  
Xiaoyong Wang ◽  
Lijuan Zhang ◽  
Qi Dai ◽  
Hongzong Si ◽  
Longyun Zhang ◽  
...  

The high concentrations of individual phytochemicals in vitro studies cannot be physiologically achieved in humans. Our solution for this concentration gap between in vitro and human studies is to combine two or more phytochemicals. We screened 12 phytochemicals by pairwise combining two compounds at a low level to select combinations exerting the synergistic inhibitory effect of breast cancer cell proliferation. A novel combination of luteolin at 30 μM (LUT30) and indole-3-carbinol 40 μM (I3C40) identified that this combination (L30I40) synergistically constrains ERα+ breast cancer cell (MCF7 and T47D) proliferation only, but not triple-negative breast cancer cells. At the same time, the individual LUT30 and I3C40 do not have this anti-proliferative effect in ERα+ breast cancer cells. Moreover, this combination L30I40 does not have toxicity on endothelial cells compared to the current commercial drugs. Similarly, the combination of LUT and I3C (LUT10 mg + I3C10 mg/kg/day) (IP injection) synergistically suppresses tumor growth in MCF7 cells-derived xenograft mice, but the individual LUT (10 mg/kg/day) and I3C (20 mg/kg/day) do not show an inhibitory effect. This combination synergistically downregulates two major therapeutic targets ERα and cyclin dependent kinase (CDK) 4/6/retinoblastoma (Rb) pathway, both in cultured cells and xenograft tumors. These results provide a solid foundation that a combination of LUT and I3C may be a practical approach to treat ERα+ breast cancer cells after clinical trials.


2012 ◽  
Vol 6 (3) ◽  
pp. 615-620 ◽  
Author(s):  
ANAN CHEN ◽  
DINGDING WANG ◽  
XUETING LIU ◽  
SHUILIAN HE ◽  
ZHIHONG YU ◽  
...  

Author(s):  
Dong-ho Bak ◽  
Seong Hee Kang ◽  
Chul-hong Park ◽  
Byung Yeoup Chung ◽  
Hyoung-Woo Bai

Abstract Chemotherapy for cancer treatment has therapeutic limitations, such as drug resistance, excessive toxic effects and undesirable adverse effects. Therefore, efforts to improve the safety and efficacy of chemotherapeutic agents are essential. Ionizing radiation can improve physiological and pharmacological properties by transforming structural modifications of the drug. In this study, in order to reduce the adverse effects of rotenone and increase anticancer activity, a new radiolytic rotenone derivative called rotenoisin A was generated through radiolytic transformation. Our findings showed that rotenoisin A inhibited the proliferation of breast cancer cells and increased the rate of apoptosis, whereas it had no inhibitory effect on primary epidermal keratinocytes compared with rotenone. Moreover, rotenoisin A-induced DNA damage by increasing reactive oxygen species (ROS) accumulation. It was also confirmed not only to alter the composition ratio of mitochondrial proteins, but also to result in structural and functional changes. The anticancer effect and molecular signalling mechanisms of rotenoisin A were consistent with those of rotenone, as previously reported. Our study suggests that radiolytic transformation of highly toxic compounds may be an alternative strategy for maintaining anticancer effects and reducing the toxicity of the parent compound.


2016 ◽  
Vol 11 (6) ◽  
pp. 3589-3596 ◽  
Author(s):  
CHANGJING CAI ◽  
XIAOQUN QIN ◽  
ZIYI WU ◽  
QIXIA SHEN ◽  
WENQIAN YANG ◽  
...  

2011 ◽  
Vol 29 (27_suppl) ◽  
pp. 220-220
Author(s):  
S. Nishiya ◽  
H. Jinno ◽  
T. Hayashida ◽  
M. Takahashi ◽  
Y. Kitagawa

220 Background: The B-cell translocation gene-2 (BTG2) belongs to a class of proteins known as the Tob and BTG antiproliferative protein family. It was shown that estrogen and progesterone suppress BTG2 expression for the development of mammary gland. We demonstrated that proliferation rate of low level BTG2 expression in MCF7 was strongly inhibited by the administration of tamoxifen. In postmenopausal breast cancer patients, androgens can be converted to mitogenic estrogens by aromatase in breast cancer cells. Based on these results, we hypothesized that BTG2 expression affects the sensitivity against aromatase inhibitior. Methods: We used tetracycline-inducible BTG2 expression model in MCF7 stably transfected with the human aromatase gene (MCF7/tet/aro) as in vitro models of aromatase-driven breast cancer. The effects of BTG2 expression and administration of anastrozole in breast cancer cells were assessed by proliferation assays. Results: Administration of androstendion increased 79.1% of cellular proliferation, suggested that introduced aromatase gene worked well. Elevated level of BTG2 mRNA expression by tetracycline treatment was confirmed by Quantitative-RTPCR. Anastrozole treatment (100nM) reduced 37.8% of cellular proliferation ability, whereas the concomitant administration of tetracycline and anastorozole reduced 59.0% of cellular proliferation. These results suggested that the inhibitory effect of anastrozol for cellular proliferation was enhanced under the condition of BTG2 expression. Conclusions: Our results suggested loss of BTG2 expression may be affects the sensitivity against aromatase inhibitor.


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