Genistein-induced neuronal apoptosis and G2/M cell cycle arrest is associated with MDC1 up-regulation and PLK1 down-regulation

Ismail, Ismail Ahmed; Kang, Ku-Seong; Lee, Hae Ahm; Kim, Jung-Wan; Sohn, Yoon-Kyung

doi:10.1016/j.ejphar.2007.07.039

Cited by 45 publications

(51 citation statements)

References 47 publications

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“…However, daidzein did not cause an arrest in the cell cycle of Caco-2 cells. In agreement with our result, genistein has been reported to induce a G2/M cell cycle arrest on human neuroblastoma SK-N-MC cells through the down-regulation of cell cycle check point proteins, Cyclin B1, Cdc2, Cdc25 and Chk2 (Ismail et al 2007). However, genistein concentrations-inducing G2/M cell cycle arrest on SK-N-MC cells, were 50 and 100 lL.…”

Section: Discussionsupporting

confidence: 93%

Genistein-induced G2/M cell cycle arrest of human intestinal colon cancer Caco-2 cells is associated with Cyclin B1 and Chk2 down-regulation

2013

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Genistein is an isoflavonic phyto-oestrogen contained in soya beans. It is thought to display anti-cancer effects. This study was designed to investigate its effect on human intestinal colon cancer Caco-2 cells. MTT assay, flow cytometric analysis and western blotting were used to investigate the effect of genistein on cell proliferation, cell cycle progression and protein alterations of selected cell cycle-related proteins in Caco-2 cells. Our results showed that genistein and daidzein significantly suppressed cell proliferation. Genistein treatment was demonstrated to modulate cell cycle distribution through accumulation of cells at G2/M phase, with a significant decreasing effect of Cyclin B1 and Serine/threonine-protein kinase 2 (Chk2) proteins expression. However, daidzein did not alter the cell cycle progression in Caco-2 cells. All these observation strongly indicate that genistein has anti-proliferative effect in human intestinal colon cancer Caco-2 cells through the downregulation of cell cycle check point proteins, Cyclin B1 and Chk2.

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Section: Discussionsupporting

confidence: 93%

Genistein-induced G2/M cell cycle arrest of human intestinal colon cancer Caco-2 cells is associated with Cyclin B1 and Chk2 down-regulation

2013

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“…In previous work, genistein was found to block reovirus protein synthesis (60), but how this occurs was not known. Genistein impairs cell cycle progression, arresting cells at the G 2 /M checkpoint by inactivating Cdc25 phosphatases (34,46,51), and induces apoptosis by an uncharacterized mechanism (51). In this study, we found that genistein produced cytostatic effects on cells (Fig.…”

Section: Discussionmentioning

confidence: 50%

Src Kinase Mediates Productive Endocytic Sorting of Reovirus during Cell Entry

Mainou

Dermody

2011

J Virol

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Reovirus cell entry is initiated by viral attachment to cell surface glycans and junctional adhesion molecule A. Following receptor engagement, reovirus is internalized into cells by receptor-mediated endocytosis using a process dependent on ␤1 integrin. Endocytosed virions undergo stepwise disassembly catalyzed by cathepsin proteases, followed by endosomal membrane penetration and delivery of transcriptionally active core particles into the cytoplasm. Cellular factors that mediate reovirus endocytosis are poorly defined. We found that both genistein, a broad-spectrum tyrosine kinase inhibitor, and PP2, a specific Src-family kinase inhibitor, diminish reovirus infectivity by blocking a cell entry step. Although neither inhibitor impedes internalization of reovirus virions, both inhibitors target virions to lysosomes. Reovirus colocalizes with Src during cell entry, and reovirus infection induces phosphorylation of Src at the activation residue, tyrosine 416. Diminished Src expression by RNA interference reduces reovirus infectivity, suggesting that Src is required for efficient reovirus entry. Collectively, these data provide evidence that Src kinase is an important mediator of signaling events that regulate the appropriate sorting of reovirus particles in the endocytic pathway for disassembly and cell entry.

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“…We next assessed the effect of Axin on the expression of p53 and its downstream genes, p21 and Cyclin D1, which are known to regulate apoptosis and cell cycle distribution (20)(21)(22). Immunoblotting and real-time PCR were using to evaluate the protein and mRNA level of p53, p21 and Cyclin D1.…”

Section: Axin Induces Apoptosis and Inhibits Proliferative Activity mentioning

confidence: 99%

Axin induces cell death and reduces cell proliferation in astrocytoma by activating the p53 pathway

Zhang

Ye²,

Zhang³

et al. 2009

Int J Oncol

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Abstract. Astrocytic tumors are the most common brain tumors with various genetic defects. As a tumor suppressor gene, Axin could control cell death and growth. Axin possesses a separate domain that directly interacts with p53 and regulates the activity of p53 pathway. Our aims were to elucidate the effects of Axin on the progression of astrocytoma. We examined the expression of Axin in 96 cases of astrocytoma using immunohistochemistry. The apoptotic index, proliferactive acitivity and the expression levels of p53 and its downstream genes, p21 and Cyclin D1, were evaluated in the C6 astrocytoma cells with overexpression or silencing of Axin. The results showed the levels of Axin correlated significantly inversely with the grades of astrocytoma (R=-0.286, P<0.05) and correlated negatively with Ki-67 labeling index (R=-0.227, P<0.05). Overexpression of Axin in C6 cells induces cell death, and reduces the cell proliferation, up-regulates the expression of p53. Silencing of Axin reduces p53 expression. The p53 inhibitor, pifithrin-·, was able to counteract the effect of Axin in C6 cells. Our data demonstrate that the expression of Axin is associated negatively with the progression of astrocytoma. In conclusion, Axin induces cell death and reduces cell proliferation, partially by activating the p53 pathway in astrocytoma cells. This knowledge is helpful in understanding the role of Axin in the progression of astrocytoma.

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Genistein-induced neuronal apoptosis and G2/M cell cycle arrest is associated with MDC1 up-regulation and PLK1 down-regulation

Cited by 45 publications

References 47 publications

Genistein-induced G2/M cell cycle arrest of human intestinal colon cancer Caco-2 cells is associated with Cyclin B1 and Chk2 down-regulation

Genistein-induced G2/M cell cycle arrest of human intestinal colon cancer Caco-2 cells is associated with Cyclin B1 and Chk2 down-regulation

Src Kinase Mediates Productive Endocytic Sorting of Reovirus during Cell Entry

Axin induces cell death and reduces cell proliferation in astrocytoma by activating the p53 pathway

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