Anticancer effects of brucine and gemcitabine combination in MCF-7 human breast cancer cells

2014 ◽  
Vol 29 (5) ◽  
pp. 484-490 ◽  
Author(s):  
Mamatha Serasanambati ◽  
Shanmuga Reddy Chilakapati ◽  
Pavan Kumar Manikonda ◽  
Jagadeeswara Reddy Kanala ◽  
Damodar Reddy Chilakapati
Processes ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 1193
Author(s):  
Hung Manh Phung ◽  
Hesol Lee ◽  
Sullim Lee ◽  
Dongyeop Jang ◽  
Chang-Eop Kim ◽  
...  

Breast cancer is the most common malignancy in both developing and developed countries. In this study, we simultaneously analyzed nine constituent compounds from Spatholobi Caulis (gallic acid, (−)-gallocatechin, 3,4-dihydroxybenzoic acid, procyanidin B1, 3,4-dihydroxybenzaldehyde, catechin, procyanidin B2, epicatechin, and (−)-epicatechin gallate) and examined their anticancer effects on MCF-7 and MDA-MB-231 human breast cancer cells. The experimental results indicated that the gallic acid showed the strongest cytotoxic effect on MCF-7 cells among tested compounds whilst most of samples did not express inhibitory effect on viability of MDA-MB-231 cells, except for 70% ethanol extract of S. Caulis. Thus, gallic acid was chosen to extend anticancer mechanism study on MCF-7 cells. Our data showed that the gallic acid induced apoptotic MCF-7 cell death through both extrinsic and intrinsic pathways, which increased the expression of cleaved caspase-7, -8, and -9, Bax and p53, but reduced the expression of Bcl-2 and poly (ADP-ribose) polymerase (PARP). In addition, the network pharmacological analysis pointed out that the p53, mitogen-activated protein kinase (MAPK), estrogen, and Wnt signaling pathways have a great correlation with the targets of gallic acid. This study suggested that gallic acid is a bioactive component of S. Caulis with potential to be used in chemotherapy for breast cancer.


2014 ◽  
Vol 31 (5) ◽  
pp. 2305-2311 ◽  
Author(s):  
MIN JEONG KIM ◽  
JI HYUN JUNG ◽  
WON SUP LEE ◽  
JEONG WON YUN ◽  
JING NAN LU ◽  
...  

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.


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