Evaluation of Induced Apoptosis by Biosynthesized Zinc Oxide Nanoparticles in MCF-7 Breast Cancer Cells Using Bak1 and Bclx Expression

2021 ◽  
Vol 500 (1) ◽  
pp. 360-367
Author(s):  
Man Yan ◽  
Mostafa Heidari Majd
2017 ◽  
Vol 104 ◽  
pp. 268-277 ◽  
Author(s):  
Balasubramanian Malaikozhundan ◽  
Baskaralingam Vaseeharan ◽  
Sekar Vijayakumar ◽  
Karuppiah Pandiselvi ◽  
Mohamed Ali Rajamohamed Kalanjiam ◽  
...  

2021 ◽  
Author(s):  
Murali Santhoshkumar ◽  
Agilan Balupillai ◽  
Ernest David

Abstract To study the biological fabrication and characterization of zinc oxide nanoparticles (ZnO NPs) using Gymnema sylvestre and their toxicity to breast cancer cells MCF-7.In the existing work, ZnO NPs were synthesized using leaf extract of the Indian medicinal plant Gymnema sylvestre and it was characterized by Particle size, Zeta potential, FT-IR, XRD and SEM analyses.This ZnO NPs to have potentially validated anticancer role in breast cancer cells MCF-7 in vitro approach.The plant-based synthesized ZnO NPs were evaluated against the inhibitory role on breast cancer cell lines. We significantly observed that ZnO-NPs induce efficient toxicity of MCF-7 cells by increasing ROS, mitochondrion membrane damage and apoptotic morphological alterations. These results stated that ZnO-NP induces Bax and Caspases and down-regulates Bcl-2 proteins in MCF-7 cells. Thus, the biologically synthesized ZnO NPs were identified as good performance to inhibit breast cancer cell growth even at low concentrations.


2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Haitham Ali Kadhem ◽  
Sumayah Abdulhussien Ibraheem ◽  
Majid Sakhi Jabir ◽  
Afraa Ali Kadhim ◽  
Zainab Jihad Taqi ◽  
...  

2015 ◽  
Vol 12 (2) ◽  
pp. 55-59
Author(s):  
Edy Meiyanto

As chemotherapeutic backbone for breast cancer therapy, doxorubicin showed various side effects and induced resistancy of breast cancer cells. Development of targeted therapy on breast cancer focused on combinatorial therapy of doxorubicin and molecular targeted agents. PGV-0 and PGV-1, a curcumin analogue showed potency as co-chemotherapeutic agent with doxorubicin. Our previous study of PGV-0 and PGV-1 showed cytotoxic activity in T47D cells. Therefore, the aim of this research is to examine the synergistic effect of PGV-0, PGV-1 on the cytotoxic activity of doxorubicin through cell cycle modulation and apoptotic induction on MCF-7 breast cancer cell lines. The cytotoxic assay of PGV-0, PGV-1, doxorubicin, and their combination were carried out by using MTT assay. Cell cycle distribution and apoptosis were determined by flowcytometer FACS-Calibur and the flowcytometry data was analyzed using Cell Quest program. Single treatment of PGV-0, PGV-1 and doxorubicin showed cytotoxic effect on MCF-7 with cell viability IC50 value 50 µM, 6 µM and 350 nM respectively. Single treatment of Doxorubicin 175 nM induced G2/M arrest. Single treatment of PGV-0 5 µM induced G2/M arrest while in higher dose 12.5  µM, PGV-0 induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 5 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 12.5 µM also increased apoptosis induction. Single treatment of PGV-1 0.6 µM induced G1 arrest while in higher dose 1.5  µM, PGV-1 induced apoptosis. Combination of doxorubicin 175 nM and PGV-1 0.6 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 1.5 µM also increased apoptosis induction. PGV-0 and PGV-1 are potential to be delevoped as co-chemotherapeutic agent for breast cancer by inducing apoptosis and cell cycle modulation, but the molecular mechanism need to be explored detail.  Key words: PGV-0, PGV-1, doxorubicin, co-chemotherapy, breast cancer, cell cycle arrest, apoptosis


2016 ◽  
Vol 151 ◽  
pp. 1027-1033 ◽  
Author(s):  
Zhiyong Luo ◽  
Xiaopeng Hu ◽  
Hua Xiong ◽  
Hong Qiu ◽  
Xianglin Yuan ◽  
...  

2004 ◽  
Vol 82 (2) ◽  
pp. 94-102 ◽  
Author(s):  
Geneviève Drouin ◽  
Annie Douillette ◽  
Pierre Lacasse ◽  
Benoit Paquette

Apoptotic pathways in breast cancer cells are frequently altered, reducing the efficiency of radiotherapy. Conjugated linoleic acid (CLA), known to trigger apoptosis, was tested as radiosensitizer in breast cancer cells MCF-7 and MDA-MB-231. The CLA-mix, made up of the isomers CLA-9cis 11trans and CLA-10trans 12cis, was compared to three purified isomers, i.e., the CLA-9cis 11cis, CLA-9cis 11trans, and CLA-10trans 12cis. Using the apoptotic marker YO-PRO®-1, the CLA-9cis 11cis at 50 µmol/L turned out to be the best apoptotic inducer leading to a 10-fold increase in MCF-7 cells and a 2,5-fold increase in MDA-MB-231 cells, comparatively to the CLA-mix. Contrary to previous studies on colorectal and prostate cancer cells, CLA-10trans 12cis does not lead to an apoptotic response on breast cancer cell lines MCF-7 and MDA-MB-231. Our results also suggest that the main components of the CLA-mix (CLA-9cis 11trans and CLA-10trans 12cis) are not involved in the induction of apoptosis in the breast cancer cells studied. A dose of 5 Gy did not induce apoptosis in MCF-7 and MDA-MB-231 cells. The addition of CLA-9cis 11cis or CLA-mix has allowed us to observe a radiation-induced apoptosis, with the CLA-9cis 11cis being about 8-fold better than the CLA-mix. CLA-9cis 11cis turned out to be the best radiosensitizer, although the isomers CLA-9cis 11trans and CLA-10trans 12cis have also reduced the cell survival following irradiation, but using a mechanism not related to apoptosis. In conclusion, the radiosensitizing property of CLA-9cis 11cis supports its potential as an agent to improve radiotherapy against breast carcinoma.Key words: breast cancer, conjugated linoleic acid (CLA), radiotherapy, apoptosis.


2004 ◽  
Vol 279 (44) ◽  
pp. 45855-45864 ◽  
Author(s):  
Xiaojian Wang ◽  
Nan Li ◽  
Bin Liu ◽  
Hongying Sun ◽  
Taoyong Chen ◽  
...  

The phosphatidylethanolamine (PE)-binding proteins (PEBPs) are an evolutionarily conserved family of proteins with pivotal biological functions. Here we describe the cloning and functional characterization of a novel family member, human phosphatidylethanolamine-binding protein 4 (hPEBP4). hPEBP4 is expressed in most human tissues and highly expressed in tumor cells. Its expression in tumor cells is further enhanced upon tumor necrosis factor (TNF) α treatment, whereas hPEBP4 normally co-localizes with lysosomes, TNFα stimulation triggers its transfer to the cell membrane, where it binds to Raf-1 and MEK1. L929 cells overexpressing hPEBP4 are resistant to both TNFα-induced ERK1/2, MEK1, and JNK activation and TNFα-mediated apoptosis. Co-precipitation andin vitroprotein binding assay demonstrated that hPEBP4 interacts with Raf-1 and MEK1. A truncated form of hPEBP4, lacking the PE-binding domain, maintains lysosomal co-localization but has no effect on cellular responses to TNFα. Given that MCF-7 breast cancer cells expressed hPEBP4 at a high level, small interfering RNA was used to silence the expression of hPEBP4. We demonstrated that down-regulation of hPEBP4 expression sensitizes MCF-7 breast cancer cells to TNFα-induced apoptosis. hPEBP4 appears to promote cellular resistance to TNF-induced apoptosis by inhibiting activation of the Raf-1/MEK/ERK pathway, JNK, and PE externalization, and the conserved region of PE-binding domain appears to play a vital role in this biological activity of hPEBP4.


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