Inhibition of the proteasome activity, a novel mechanism associated with the tumor cell apoptosis-inducing ability of genistein

Kazi, Aslamuzzaman; Daniel, Kenyon G.; Smith, David M.; Kumar, Nagi B.; Dou, Q. Ping

doi:10.1016/s0006-2952(03)00414-3

Cited by 152 publications

(133 citation statements)

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“…Resveratrol has been demonstrated to suppress cytokine-induced proteasome function and degradation of IkBa (42). Genistein is thought to interact with the proteasomal ␤5 subunit and result in the inhibition of the chymotrypsin-like activity of the proteasome (43). After 2 h of pretreatment, cells were infected with MP-12 virus.…”

Section: Inhibition Of the Ikk Complex Resulted In Decreased Viralmentioning

confidence: 99%

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Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Narayanan

Kehn-Hall

Senina

et al. 2012

Journal of Biological Chemistry

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Background: Rift Valley fever virus is a single-stranded RNA virus that causes disease in humans and livestock. Results: Rift Valley fever virus infection activates the host NFB signaling cascade. Conclusion: NFB inhibitors, particularly curcumin, down-regulate virus in both in vitro and in vivo models. Significance: Novel versions of host components resulting from an infection make them ideal therapeutic targets.

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Section: Inhibition Of the Ikk Complex Resulted In Decreased Viralmentioning

confidence: 99%

“…3 and 4). Thus, it is possible that the novel IKK-␤2 complex observed in RVFV-infected cells is a hyperactive enzyme that lacks the control that could be exerted normally on the IKK-␤ complex (43).…”

Section: Mice a Infarmentioning

confidence: 99%

Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Narayanan

Kehn-Hall

Senina

et al. 2012

Journal of Biological Chemistry

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“…These results suggest that the induction of p21 WAF1 and apoptosis by genistein is functionally operated through a p53-independent pathway. A study reported by Kazi et al [48] showed that genistein induced apoptosis by inhibiting proteosome and induction of p27 KIP1 , IκBα, and Bax. A recent study showed that in hepatocellular carcinoma, genistein induced apoptosis by the activation of several endoplasmic reticulum (ER) stress-relevant regulators, which include the transcription factor-GADD153, m-calpain, GRP78 and caspase-12 [49].…”

Section: Effects On the Induction Of Apoptosismentioning

confidence: 97%

Multi-targeted therapy of cancer by genistein

Banerjee¹,

Li²,

Wang³

et al. 2008

Cancer Letters

560

383

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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.

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“…Genistein, a soy isoflavone, inhibited the proteasomal chymotrypsin-like activity in vitro and in vivo in prostate cancer (LNCaP) and breast cancer (MCF-7) cells (59). The ester bond-containing tea polyphenols, such as epigallocatechin-3-gallate (EGCG), and the dietary polyphenol known as tannic acid (TA), inhibited the proteasome activity in vitro and in vivo at the concentrations found in the serum of green tea drinkers (60).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Proteasome Activity by Vitamin E in THP‐1 Monocytes

et al. 2007

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SummaryIn THP-1 monocytes, cellular proteasome inhibition by ritonavir or ALLN is associated with increased production of oxidative stress. Both compounds produced comparable amounts of oxidative stress; however, normalization by a-tocopherol occurred solely after inhibition by ritonavir, and not by ALLN. Similar to that, atocopherol could normalize the reduced formation of 3-nitrotyrosine-modified proteins only after ritonavir treatment. In the absence of any proteasome inhibitor, intrinsic cellular proteasome activity was not modulated by a-, b-, and g-tocopherols; however, dtocopherol, a-tocotrienol, and a-tocopheryl phosphate could significantly inhibit cellular proteasome activity and increased the level of p27Kip1 and p53. Since oxidative stress was reduced by atocopherol only after proteasome inhibition by ritonavir and not by ALLN, it is concluded that, in this experimental system, atocopherol does not act as an antioxidant but interferes with the inhibitory effect of ritonavir. IUBMB Life, 59: 771-780, 2007

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Inhibition of the proteasome activity, a novel mechanism associated with the tumor cell apoptosis-inducing ability of genistein

Cited by 152 publications

References 50 publications

Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Multi-targeted therapy of cancer by genistein

Modulation of Proteasome Activity by Vitamin E in THP‐1 Monocytes

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