Induction of apoptosis in breast cancer cells MDA-MB-231 by genistein

Li, Yiwei; Upadhyay, Sunil; Bhuiyan, M. S. A.; Sarkar, Fazlul H.

doi:10.1038/sj.onc.1202650

Cited by 289 publications

(222 citation statements)

References 43 publications

(43 reference statements)

Supporting

Mentioning

200

Contrasting

Order By: Relevance

“…[18][19][20][21][22][23][24][25] Previous studies reported from our laboratory have shown that genistein regulates genes that are related in controlling cell proliferation, cell cycle, apoptosis, oncogenesis, transcription regulation, angiogenesis, and cancer cell invasion and metastasis. [26][27][28][29][30] We have also shown that genistein inhibits NF-jB activation, which is partly mediated via Akt signaling pathway. 31 We therefore hypothesize that genistein may alter the sensitivity of pancreatic cancer cells to conventional therapies by overcoming de novo as well as acquired chemoresistance due to inactivation of NF-jB during chemotherapy.…”

mentioning

confidence: 99%

Retracted: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer

Banerjee

Zhang

Wang

et al. 2006

Intl Journal of Cancer

View full text Add to dashboard Cite

We recently reported the potential of genistein in augmenting gemcitabine-induced killing of pancreatic cancer (Banerjee, S. et al., Cancer Research 2005;65:9064-72). Since cis-diaminedichloroplatinum (II) (cisplatin) is widely used against solid tumors, we further investigated whether genistein pretreatment could be used as a novel strategy for cisplatin-induced killing of pancreatic cancer cells in vitro and enhanced antitumor activity in vivo. Our in vitro results showed that pretreatment of cells with genistein followed by cisplatin resulted in significant loss of cell viability and potentiated apoptosis irrespective of the metastatic ability of cells. Mechanistically, genistein augmented cisplatin induced killing by down regulating transcription factor-NF-jB and anti-apoptotic Akt expression. NF-jB was found upregulated when pancreatic cancer cells were exposed to cisplatin, suggesting the potential mechanism of acquired chemo-resistance. In addition, we also showed, for the first time, that genistein in combination with cisplatin is more effective antitumor agent in our orthotopic tumor model. But most importantly, our data also showed that a specific target, such as NF-jB, was inactivated in animal tumors treated with genistein and cisplatin. Immunohistochemical data showed reduced staining for phospho-p65, Bcl-xL and MMP-9 in treated tumors compared to control tumors, but the lowest activity was seen in the combination group. These results provide strong molecular in vivo evidence in support of our hypothesis that inactivation of the NF-jB signaling pathway by genistein results in the chemo-sensitization of pancreatic tumors to cisplatin, which is likely to be an important and novel strategy for the treatment of pancreatic cancer. ' 2006 Wiley-Liss, Inc.

show abstract

mentioning

confidence: 99%

Retracted: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer

Banerjee

Zhang

Wang

et al. 2006

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…3,4 It has been found that genistein can inhibit the growth of various cancer cell lines both in vitro and in vivo. [5][6][7][8][9][10] Our previous studies also showed that genistein can induce apoptosis and inhibit NF-jB activation in pancreatic cancer cells. 8,9,11 NF-jB plays important roles in the control of cell growth, differentiation, apoptosis and inflammation.…”

mentioning

confidence: 99%

Retracted: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells

Wang

Zhang

Banerjee

et al. 2005

Intl Journal of Cancer

Self Cite

118

View full text Add to dashboard Cite

This article has been retracted at the request of: Editor‐in‐Chief and Author ‘Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells’, by Wang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H. The above article and associated erratum, published online on 11 November 2005 and 6 February 2014, respectively, in Wiley Online Library (http://wileyonlinelibrary.com), have been retracted by agreement between the authors, the journal Editor‐in‐Chief, Professor Peter Lichter, and Wiley Periodicals, Inc. In addition to what was corrected in the erratum, a university investigation involving the first and the corresponding author determined that several figures in this paper were re‐used, mislabeled, manipulated, or duplicated while processing/compiling the final figures assembled from the original data sources. Therefore, the authors are retracting the paper in its entirety although they maintain that these issues did not affect the major conclusions. They apologize for any inconvenience this may have caused. Reference Wang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H. (2006), Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 118:1930–1936. doi:10.1002/ijc.21589; corrected by Erratum: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 134: E3. doi: .

show abstract

“…Furthermore, the p53 and p21 WAF1 tumor suppressor genes are also known to be involved in apoptotic processes, and we have detected the expression of p53 gene in MDA-MB-231 breast cancer cells, which are ER-negative and harbor mutant p53. Although the treatment of these cells with genistein downregulated the expression of the dysfunctional p53, the expression of p21 WAF1 was induced within 24 h [37]. These results suggest that the induction of p21 WAF1 and apoptosis by genistein is functionally operated through a p53-independent pathway.…”

Section: Effects On the Induction Of Apoptosismentioning

confidence: 53%

Multi-targeted therapy of cancer by genistein

Banerjee¹,

Li²,

Wang³

et al. 2008

Cancer Letters

Self Cite

548

383

View full text Add to dashboard Cite

Soy isoflavones have been identified as dietary components having an important role in reducing the incidence of breast and prostate cancers in Asian countries. Genistein, the predominant isoflavone found in soy products, has been shown to inhibit the carcinogenesis in animal models. There is a growing body of experimental evidence showing that the inhibition of human cancer cell growth by genisteinis mediated via the modulation of genes that are related to the control of cell cycle and apoptosis. It has been shown that genistein inhibits the activation of NF-κB and Akt signaling pathways, both of which are known to maintain a homeostatic balance between cell survival and apoptosis. Moreover, genistein antagonizes estrogen-and androgen-mediated signaling pathways in the processes of carcinogenesis. Furthermore, genistein has been found to have antioxidant properties, and shown to be a potent inhibitor of angiogenesis and metastasis. Taken together, both in vivo and in vitro studies have clearly shown that genistein, one of the major soy isoflavones, is a promising agent for cancer chemoprevention and further suggest that it could be an adjunct to cancer therapy by virtue of its effects on reversing radioresistance and chemoresistance. In this review, we attempt to provide evidence for these preventive and therapeutic effects of genistein in a succinct manner highlighting comprehensive state-of-the-art knowledge regarding its multi-targeted biological and molecular effects in cancer cells.

show abstract

Induction of apoptosis in breast cancer cells MDA-MB-231 by genistein

Cited by 289 publications

References 43 publications

Retracted: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer

Retracted: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer

Retracted: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells

Multi-targeted therapy of cancer by genistein

Contact Info

Product

Resources

About