scholarly journals Antiproliferative Activity Evaluation of a Series ofN-1,3-Benzothiazol-2-ylbenzamides as Novel Apoptosis Inducers

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Filomena Corbo ◽  
Alessia Carocci ◽  
Domenico Armenise ◽  
Nicolino De Laurentis ◽  
Antonio Laghezza ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Antiproliferative Activity ◽  
Human Breast Cancer ◽  
Human Liver ◽  
Inhibitory Effect ◽  
Human Breast ◽  
Liver Hepatocellular Carcinoma ◽  
Mcf 7

A series ofN-1,3-benzothiazol-2-ylbenzamide derivatives were studied for their antiproliferative activity on human liver hepatocellular carcinoma (HepG2) and human breast cancer (MCF-7) cell lines. Most of them were found to show a prominent inhibitory effect on cell growth. Among the most active compounds,1kemerged for its proapoptotic effect that is particularly evident towards MCF-7 cancer cell lines.

scholarly journals Antiproliferative activity of natural coumarins from Calophyllum incrasaptum M.R Henderson-Wyatt Smith against human breast cancer cells MCF

2018 ◽  
Vol 154 ◽  
pp. 04003
Author(s):  
Jamilah Abbas ◽  
Linar Z Udin ◽  
Muhammad Hanafi
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Antiproliferative Activity ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Alamar Blue ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

Objective: to evaluated the antiproliferative activity of natural coumarin from Calophyllum incrasaptum M.R Henderson-Wytt Smith against human breast cancer cells MCF-7. Methode : Coumarin from ethyl acetate fraction of C. incrasaptum M.R Henderson-Wyatt Smith was isolated by coloumn chromatographyic and structure elucidated by using spectroscopic methods and isolate compound was evaluated for their antiproliferative activities in the alamar blue assay. Result: Coumarin have antiproliferative activity against MCF-7 cancer cell lines through alamar blue assay for 4 h after treatment. Conclusions: coumarin showed good activity against cancer cell lines with IC50 value of 2.23 μg/mL.

scholarly journals Involvement of PPARα in the growth inhibitory effect of arachidonic acid on breast cancer cells

2008 ◽  
Vol 100 (4) ◽  
pp. 739-750 ◽  
Author(s):  
Claudia Bocca ◽  
Francesca Bozzo ◽  
Germana Martinasso ◽  
Rosa Angela Canuto ◽  
Antonella Miglietta
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Human Breast Cancer ◽  
Inhibitory Effect ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Growth Inhibitory Effect ◽  
Growth Inhibitory ◽  
Mcf 7

Epidemiological studies suggest that dietary PUFA may influence breast cancer progression. n-3 PUFA are generally known to exert antitumour effects, whereas reports relative to n-6 PUFA anti-carcinogen effects are controversial. Arachidonic acid (AA; 20 : 4n − 6) and its metabolites have been shown to inhibit the growth of human breast cancer cell lines, even if the downstream mechanisms by which AA may influence carcinogenesis remain unresolved. We explored the molecular basis for AA influence on proliferation, signal transduction and apoptosis in two human breast cancer cell lines, MCF-7 and MDA-MB-231. In both cell lines AA inhibited cell growth in a dose-dependent manner, even if MDA-MB-231 was somewhat more growth-inhibited than MCF-7. AA decreased extracellular signal-regulated protein kinase 1/2 phosphorylation level, and positively modulated PPARγ and PPARα expression, with only a slight effect against PPARβ/δ. In addition, AA increased Bak (an apoptosis-regulating protein) expression and reduced procaspase-3 and -9 levels only in MDA-MB-231 cells, thus indicating that the growth inhibitory effect can be correlated with apoptosis induction. In both cell lines the use of a specific antagonist made it possible to establish a relationship between AA growth inhibitory effect and PPARα involvement. AA decreases cell proliferation most likely by inducing apoptosis in MDA-MB-231 cells, while in the MCF-7 cell line the growth inhibitory activity can be attributed to the inhibition of the signal transduction pathway involved in cell proliferation. In both cases, the results here presented suggest PPARα as a possible contributor to the growth inhibitory effect of AA.

scholarly journals Antiproliferative activity of ionic liquid-graviola fruit extract against human breast cancer (MCF-7) cell lines using flow cytometry techniques

2019 ◽  
Vol 236 ◽  
pp. 466-473 ◽  
Author(s):  
Djabir Daddiouaissa ◽  
Azura Amid ◽  
Nassereldeen A. Kabbashi ◽  
Fazia A.A. Fuad ◽  
AhmedA.M. Elnour ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Flow Cytometry ◽  
Ionic Liquid ◽  
Cell Lines ◽  
Antiproliferative Activity ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Fruit Extract ◽  
Mcf 7

scholarly journals Antiestrogen-resistant human breast cancer cells require activated Protein Kinase B/Akt for growth

2005 ◽  
Vol 12 (3) ◽  
pp. 599-614 ◽  
Author(s):  
T Frogne ◽  
J S Jepsen ◽  
S S Larsen ◽  
C K Fog ◽  
B L Brockdorff ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Cell Lines ◽  
Human Breast Cancer ◽  
Neutralizing Antibodies ◽  
Breast Cancer Cells ◽  
Resistant Cell ◽  
Breast Cancer Patients ◽  
Human Breast ◽  
Mcf 7

Development of acquired resistance to antiestrogens is a major clinical problem in endocrine treatment of breast cancer patients. The IGF system plays a profound role in many cancer types, including breast cancer. Thus, overexpression and/or constitutive activation of the IGF-I receptor (IGF-IR) or different components of the IGF-IR signaling pathway have been reported to render breast cancer cells less estrogen dependent and capable of sustaining cell proliferation in the presence of antiestrogens. In this study, growth of the antiestrogen-sensitive human breast cancer cell line MCF-7 was inhibited by treatment with IGF-IR-neutralizing antibodies. In contrast, IGF-IR-neutralizing antibodies had no effect on growth of two different antiestrogen-resistant MCF-7 sublines. A panel of antiestrogen-resistant cell lines was investigated for expression of IGF-IR and either undetectable or severely reduced IGF-IR levels were observed. No increase in insulin receptor substrate 1 (IRS-1) or total PKB/Akt (Akt) was detected in the resistant cell lines. However, a significant increase in phosphorylated Akt (pAkt) was found in four of six antiestrogen-resistant cell lines. Overexpression of pAkt was associated with increased Akt kinase activity in both a tamoxifen- and an ICI 182,780-resistant cell line. Inhibition of Akt phosphorylation by the phosphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin or the Akt inhibitor SH-6 (structurally modified phosphatidyl inositol ether liquid analog PIA 6) resulted in a more pronounced growth inhibitory effect on the antiestrogen-resistant cells compared with the parental cells, suggesting that signaling via Akt is required for antiestrogen-resistant cell growth in at least a subset of our antiestrogen-resistant cell lines. PTEN expression and activity was not decreased in cell lines overexpressing pAkt. Our data demonstrate that Akt is a target for treatment of antiestrogen-resistant breast cancer cell lines and we suggest that antiestrogen-resistant breast cancer patients may benefit from treatment targeted to inhibit Akt signaling.

scholarly journals Antiproliferative Activity of Combined Biochanin A and Ginsenoside Rh2 on MDA-MB-231 and MCF-7 Human Breast Cancer Cells

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2908 ◽  
Author(s):  
Guixing Ren ◽  
Zhenxing Shi ◽  
Cong Teng ◽  
Yang Yao
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Human Breast Cancer ◽  
Synergistic Effects ◽  
Inhibitory Effect ◽  
Biochanin A ◽  
Migration And Invasion ◽  
Ginsenoside Rh2 ◽  
Human Breast ◽  
Mcf 7

Breast cancer is the most frequently diagnosed cancer in women worldwide. The antiproliferative activities of biochanin A (BA) and ginsenoside Rh2 were determined by evaluating their inhibitory effect on MDA-MB-231 human breast cancer cell proliferation. The combination of BA with Rh2 was also assessed. In MDA cells, combination treatment led to a decrease in the EC50 values of BA and Rh2 to 25.20 μM and 22.75 μM, respectively. In MCF-7 cells, the EC50 values of combined BA and Rh2 decreased to 27.68 μM and 25.41 μM, respectively. BA combined with Rh2 also improved the inhibition of MDA-MB-231 and MCF-7 cell migration and invasion compared to the individual compounds. Western blot analysis demonstrated upregulation in p-p53, p-p38, and p-ASK1 proteins while levels of TRAF2 were downregulated. These results suggest that BA combined with Rh2 exhibits synergistic effects against MDA-MB-231 and MCF-7 cell proliferation.

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