scholarly journals Selective cytotoxicity of a Vietnamese traditional formula, Nam Dia long, against MCF-7 cells by synergistic effects

Author(s):  
My-Nuong Thi Nguyen ◽  
Thuy-Duong Ho-Huynh
Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2908 ◽  
Author(s):  
Guixing Ren ◽  
Zhenxing Shi ◽  
Cong Teng ◽  
Yang Yao

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.


1993 ◽  
Vol 18 (4) ◽  
pp. 269-274 ◽  
Author(s):  
Yong J. Lee ◽  
Zi-Zheng Hou ◽  
LindaLi Curetty ◽  
Joong M. Cho ◽  
Peter M. Corry
Keyword(s):  
Ht 29 ◽  

2011 ◽  
Vol 02 (03) ◽  
pp. 394-400 ◽  
Author(s):  
Shahnaz Khaghani ◽  
Farideh Razi ◽  
Mohsen Mohammadian Yajloo ◽  
Malihe Paknejad ◽  
Ahmad Shariftabrizi ◽  
...  

2016 ◽  
Vol 89 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Flaviu Drigla ◽  
Ovidiu Balacescu ◽  
Simona Visan ◽  
Simona Elena Bisboaca ◽  
Ioana Berindan-Neagoe ◽  
...  

Background and aims. Breast cancer is a heterogeneous disease and the leading cause of cancer mortality worldwide. Triple negative breast cancer (TNBC) is considered to be one of the most aggressive breast neoplasia due to failure of chemotherapy response. Thus, there is an urgent need of finding alternative therapies for TNBC. This study was designed to evaluate the synergistic effect induced by propolis and bee venom on luminal (MCF-7) and TNBC (Hs578T) cell lines. Methods. In order to evaluate the synergistic effect of aqueous extract of propolis and bee venom, we treated in combination two breast cancer cell lines: MCF-7(luminal subtype) and Hs578T (TNBC subtype).Results. Our results indicate that both cell lines exhibited similar sensitivity to the aqueous extract of propolis at a dilution of 0.072-0.09 mg/ml. The results concerning IC50 forbee venom on MCF-7 cells was 1 mg/ml, 20 times higher than 0.05 mg/ml in Hs578T cells. By combining the aqueous extract of propolis with bee venom, we obtained synergistic effects at a higher concentration, which was 5 and 2 times stronger than the two treatments alone.Conclusion. Overall, the results from our study indicated that the combination of aqueous extract of propolis and bee venom treatments induced synergistic antiproliferative effects in a concentration-dependent manner in breast cancer cells. Thus we can hypothesize that the combination of honeybee propolis and venom might be involved in signaling pathways that could overcome cells resistance to therapy.


2015 ◽  
Vol 33 (28_suppl) ◽  
pp. 135-135
Author(s):  
Ye-Won Jeon ◽  
Youngjin Suh

135 Background: The anti-cancer effects of celecoxib and luteolin are well known. Although our previous study demonstrated that the combination of celecoxib and luteolin synergistically inhibits breast tumor growth compared with each of the treatments alone, we did not uncover the molecular mechanisms of these effects. The aims of our present study were to compare the effects of a celecoxib and luteolin combination treatment in four different human breast cell lines and to determine the mechanisms of action in vitro and in vivo. Methods: Using MCF-7, MCF7/HER18, MDA-MB-231 and SkBr3 human breast cancer cells, proliferation assay, apoptosis assay, inhibition assay with MEK and PI3K inhibitor in addition to western blotting and xenograft study after treatment with celecoxib and luteolin. Results: The synergistic effects of a celecoxib and luteolin combination treatment yielded significantly greater cell growth inhibition in all four breast cancer cell lines compared with the single agents alone. In particular, combined celecoxib and luteolin treatment significantly decreased the growth of MDA-MB-231 cancer cells in vivo compared with either agent alone. The celecoxib and luteolin combination treatment induced synergistic effects via Akt inactivation and extracellular signal-regulated kinase (ERK) signaling inhibition in MCF-7 and MCF7/HER18 cells and via Akt inactivation and ERK signaling activation in MDA-MB-231 and SkBr3 cells. Conclusions: These results demonstrate the synergistic anti-tumor effect of the celecoxib and luteolin combination treatment in different four breast cancer cell lines, thus introducing the possibility of this combination as a new treatment modality.


2004 ◽  
Vol 85 (1) ◽  
pp. 65-79 ◽  
Author(s):  
Fatima Hakimuddin ◽  
Gopinadhan Paliyath ◽  
Kelly Meckling

2010 ◽  
Vol 13 (2) ◽  
pp. 136 ◽  
Author(s):  
Jia Guo ◽  
Wan-Liang Lu

PURPOSE: The cancer stem cells play an important role in the invasion, metastasis and relapse of cancers as they are resistant to regular chemotherapy. In the present study, stealth liposomal daunorubicin plus tamoxifen was developed for eradicating breast cancer cells together with cancer stem cells. METHODS: Inhibitory effects were performed on the bulk human breast cancer cells (MCF-7), the sorted MCF-7 cancer stem-like cells (side population, SP), and the sorted MCF-7 cancer cells (NSP), respectively. Antitumor activity and TUNEL analysis were evaluated on the MCF-7 xenografts in nude mice. RESULTS: The encapsulation efficiencies of daunorubicin and tamoxifen were 95% and 90%, respectively. The mean particle size of the stealth liposomes was about 100 nm. Breast cancer stem cells were identified by the specific markers CD44+/CD24-, and isolated from bulk MCF-7 cells. When applying stealth liposomal daunorubicin plus tamoxifen, the inhibitory effects on both the breast cancer cells and the cancer stem cells were significantly increased in vitro, respectively. In the MCF-7 xenografts in mice, stealth liposomal daunorubicin plus tamoxifen showed the most favorable antitumor activity due to the passive targeting the tumor tissue and the synergistic effects in eliminating breast cancer cells and cancer stem cells. CONCLUSION: Stealth liposomal daunorubicin plus tamoxifen could have the potentials in eliminating both breast cancer cells and cancer stem cells.


2015 ◽  
Vol 35 (2) ◽  
pp. 912-922 ◽  
Author(s):  
YING-ZI FU ◽  
YUAN-YUAN YAN ◽  
MIAO HE ◽  
QING-HUAN XIAO ◽  
WEI-FAN YAO ◽  
...  

2015 ◽  
Vol 35 (4) ◽  
pp. 1499-1526 ◽  
Author(s):  
Xiao Xing Stander ◽  
Barend André Stander ◽  
Annie Margaretha Joubert

Background: C9, a newly in silico-designed inhibitor of microtubule dynamics induces G2/M arrest culminating in apoptosis. Dichloroacetate (DCA) inhibits pyruvate dehydrogenase kinase, an enzyme that promotes pyruvate entry into mitochondria. The use of antitumor drugs targeting different cancer features can be a more effective way to overcome drug resistance. Methods: The influence of C9 (130 nM) + DCA (7.5 mM) on MCF-7 and MCF-12 cells was assessed via microscopy spectrophotometry global gene expression and flow cytometry assays. Results: An LDH assay showed that C9+DCA treatment decreased cell viability to 83.5% in MCF-7 cells when compared to the non-tumorigenic MCF-12A cells 92.4% (P < 0.05). C9- and C9+DCA treatment induced mitochondrial membrane potential depolarization in MCF-7 cells but not in MCF-12A cells (P < 0.05). The occurrence of apoptosis was associated with increased hypo- and hyper-phosphorylation of Bcl-2 Ser70 and caspase 7 activation. Kinase inhibition revealed sustained activation of the JNK pathway caused increased Bcl-2 protein Ser70 hypo-and hyper-phosphorylation. Elevated levels of DCF fluorescence was observed in DCA-, C9- and C9+DCA-exposed MCF-7 cells, but not in MCF-12A cells, indicating cytosolic H2O2/Fe2+ formation in treated tumorigenic cells. LC3-II expression was elevated in C9+DCA-treated cells in both cell lines, indicating that autophagy was also induced. Conclusions: Synergistic effects of C9+DCA were demonstrated on breast carcinoma and non-tumorigenic cells with selectivity towards the MCF-7 cells. Antimitotic compound C9 in combination with a glycolytic inhibitor dichloroacetate eradicates breast cancer cells through ROS-JNK-Bcl-2-mediated signalling pathways in vitro and it is argued that autophagy acts as protective mechanism in the treated cells before apoptosis occurs.


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