Apoptotic effect of lambertianic acid through AMPK/FOXM1 signaling in MDA-MB231 breast cancer cells

2018 ◽  
Vol 32 (9) ◽  
pp. 1755-1763 ◽  
Author(s):  
Jae Hee Lee ◽  
Hyo-Jung Lee ◽  
Deok Yong Sim ◽  
Ji Hoon Jung ◽  
Ka Ram Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Apoptotic Effect ◽  
Lambertianic Acid

EGFR-independent Elk1/CIP2A signalling mediates apoptotic effect of an erlotinib derivative TD52 in triple-negative breast cancer cells

2017 ◽  
Vol 72 ◽  
pp. 112-123 ◽  
Author(s):  
Chun-Yu Liu ◽  
Tzu-Ting Huang ◽  
Chun-Teng Huang ◽  
Ming-Hung Hu ◽  
Duen-Shian Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Apoptotic Effect

Sensitization of MCF-7 breast cancer cells to the apoptotic effect of estradiol

2006 ◽  
Vol 141 (3) ◽  
pp. 357-360 ◽  
Author(s):  
A. M. Shcherbakov ◽  
Yu. S. Lobanova ◽  
V. A. Shatskaya ◽  
O. V. Onopchenko ◽  
A. V. Gaspar’yan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Apoptotic Effect ◽  
Mcf 7

scholarly journals FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1288 ◽  
Author(s):  
Young-Ho Kim ◽  
Hyun-Kyoung Kim ◽  
Hee Yeon Kim ◽  
HyeRan Gawk ◽  
Seung-Hyun Bae ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Candidate Genes ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Xenograft Model ◽  
Predictive Marker ◽  
Marker Genes ◽  
Mouse Xenograft Model ◽  
Apoptotic Effect

Background: Cancers with copy-gain drug-target genes are excellent candidates for targeted therapy. In order to search for new predictive marker genes, we investigated the correlation between sensitivity to targeted drugs and the copy gain of candidate target genes in NCI-60 cells. Methods: For eight candidate genes showing copy gains in NCI-60 cells identified in our previous study, sensitivity to corresponding target drugs was tested on cells showing copy gains of the candidate genes. Results: Breast cancer cells with Focal Adhesion Kinase (FAK)-copy-gain showed a significantly higher sensitivity to the target inhibitor, FAK inhibitor 14 (F14). In addition, treatment of F14 or FAK-knockdown showed a specific apoptotic effect only in breast cancer cells showing FAK-copy-gain. Expression-profiling analyses on inducible FAK shRNA-transfected cells showed that FAK/AKT signaling might be important to the apoptotic effect by target inhibition. An animal experiment employing a mouse xenograft model also showed a significant growth-inhibitory effect of F14 on breast cancer cells showing FAK-copy-gain, but not on those without FAK-copy-gain. Conclusion: FAK-copy-gain may be a predictive marker for FAK inhibition therapy in breast cancer.

miR-155-5p antagonizes the apoptotic effect of bufalin in triple-negative breast cancer cells

2016 ◽  
Vol 27 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Qian Wang ◽  
Ce Li ◽  
Zhitu Zhu ◽  
Yuee Teng ◽  
Xiaofang Che ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Apoptotic Effect

Apoptotic Effect of Koumine on Human Breast Cancer Cells and the Mechanism Involved

2015 ◽  
Vol 72 (2) ◽  
pp. 411-416 ◽  
Author(s):  
Xiaohua Zhang ◽  
Yi Chen ◽  
Bo Gao ◽  
Donglin Luo ◽  
Yayuan Wen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Apoptotic Effect

scholarly journals Anti-proliferative and apoptotic effect of tetrahydrobenzo[h]quinoline on MCF-7 human breast cancer cell

2021 ◽  
Author(s):  
Maryam Ghaffari ◽  
Dariush Shanehbandi ◽  
Solmaz Sarhadi ◽  
Mina Hanifeh Ahagh ◽  
Mahsa Maleki Moghaddam ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Expression Level ◽  
Caspase 8 ◽  
Human Breast ◽  
Caspase 9 ◽  
Anti Cancer ◽  
Apoptotic Effect ◽  
Mcf 7

Background: Quinoline and its derivatives display various biological activities based on versatility in designing a new drug class for medicinal applications. Hence, synthesizing innovative and varied derivatives of quinoline has gained considerable attention among chemists and biologists. This study evaluated the anti-proliferative and apoptotic effect of tetrahydrobenzo[h]quinoline on Michigan Cancer Foundation-7 (MCF-7) human breast cancer cells. Methods: The anti-proliferative effect of tetrahydrobenzo[h]quinoline was studied via MTT [3 0-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide] assays. A quantitative and qualitative study of apoptosis was carried out via flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Quantitative real-time PCR (qPCR) and immunoblotting analysis were employed to identify the expression level of genes and proteins involved in the apoptosis signaling pathway. Results: The synthesized compound reduced 50% of cell growth at concentrations of 10 and 7.5 µM during 24 and 48h, respectively, and induced apoptosis up to 30% in MCF-7 cancer cells. Regarding the gene expression level, Bcl-2 displayed considerable alleviation, whereas Bax expression increased significantly. Despite the remarkable increase in caspase 9 expression, there was no noticeable difference in the caspase 8 expression in treated cells compared to the control group. Western blotting data showed that the protein expression level of Bcl-2, pro-caspase 8, and 9 reduced. The protein content of Bax, cleaved-caspase 8, and 9 increased significantly, of which the protein level of cleaved-caspase 9 exhibited a tremendous rise in the treated group. Conclusion: The newly synthesized tetrahydrobenzo[h]quinoline can be a promising organic compound for cancer treatment if its anti-cancer effect investigates by other types of breast cancer cells. In vivo studies should be used to investigate the anti-cancer efficiency of this compound.

Mediation of HER2 expression-dependent antiproliferative and pro-apoptotic effect of pan-HER2-specific TKIs on breast cancer cells through STAT5 and JNK.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e11606-e11606
Author(s):  
Daphne Gschwantler-Kaulich
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Her2 Expression ◽  
Her Family ◽  
Proliferation And Apoptosis ◽  
Apoptotic Effect

e11606 Background: HER-targeted tyrosine kinase inhibitors (TKIs) have demonstrated pro-apoptotic and antiproliferative effects in vitro and in vivo. The exact pathways through which TKIs exert their antineoplastic effects are, however, still not completely understood. Methods: Using Milliplex assays, we have investigated the effects of the three panHER-TKIs lapatinib, canertinib and afatinib on signal transduction cascade activation in SKBR3, T47D and Jurkat neoplastic cell lines. The growth-inhibitory effect of blockade of HER and of JNK and STAT5 signaling was measured by proliferation- and apoptosis-assays using formazan dye labeling of viable cells, Western blotting for cleaved PARP and immunolabeling for active caspase 3, respectively. Results: All three HER-TKIs clearly inhibited proliferation and increased apoptosis in HER2 overexpressing SKBR3 cells, while their effect was less pronounced on HER2 moderately expressing T47D cells where they exerted only a weak antiproliferative and essentially no pro-apoptotic effect. Remarkably, phosphorylation/activation of JNK and STAT5A/B were inhibited by HER-TKIs only in the sensitive, but not in the resistant cells. In contrast, phosphorylation/activation of ERK/MAPK, STAT3, CREB, p70 S6 kinase, IkBa, and p38 were equally affected by HER-TKIs in both cell lines, irrespective of their sensitivity against the HER-TKIs. Moreover, we demonstrated that direct pharmacological blockade of JNK and STAT5 abrogates cell growth in both HER-TKI-sensitive as well as -resistant breast cancer cells, respectively. Conclusions: We have shown that HER-TKIs exert a HER2 expression-dependent effect on proliferation and apoptosis in cancer cell lines in vitro, which is at least partially mediated by blockade of JNK and STAT5A/B. Despite slight differences in their specificity towards individual members of the HER family all three inhibitors had comparable antiproliferative and proapoptotic effects in vitro.

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