Pleiotropic effects of genistein in metabolic, inflammatory, and malignant diseases

Nagaraju, Ganji Purnachandra; Zafar, Syed F.; El‐Rayes, Bassel F.

doi:10.1111/nure.12044

Cited by 73 publications

(37 citation statements)

References 143 publications

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“…Soy isoflavonoids also exhibit anti-angiogenic activities, but the precise mechanism of inhibition remains unclear. These compounds exert anti-angiogenic effect either directly through endothelial cells (EC) or indirectly by modulating the tumor microenvironment [79,80,81]. …”

Section: Antiangiogenic Effect Of Soy Isoflavonoidsmentioning

confidence: 99%

Soy and Breast Cancer: Focus on Angiogenesis

Varinská

Gál

Mojžišová

et al. 2015

IJMS

161

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Epidemiological studies have revealed that high consumption of soy products is associated with low incidences of hormone-dependent cancers, including breast and prostate cancer. Soybeans contain large amounts of isoflavones, such as the genistein and daidzain. Previously, it has been demonstrated that genistein, one of the predominant soy isoflavones, can inhibit several steps involved in carcinogenesis. It is suggested that genistein possesses pleiotropic molecular mechanisms of action including inhibition of tyrosine kinases, DNA topoisomerase II, 5α-reductase, galectin-induced G2/M arrest, protein histidine kinase, and cyclin-dependent kinases, modulation of different signaling pathways associated with the growth of cancer cells (e.g., NF-κB, Akt, MAPK), etc. Moreover, genistein is also a potent inhibitor of angiogenesis. Uncontrolled angiogenesis is considered as a key step in cancer growth, invasion, and metastasis. Genistein was found to inhibit angiogenesis through regulation of multiple pathways, such as regulation of VEGF, MMPs, EGFR expressions and NF-κB, PI3-K/Akt, ERK1/2 signaling pathways, thereby causing strong antiangiogenic effects. This review focuses on the antiangiogenic properties of soy isoflavonoids and examines their possible underlying mechanisms.

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Section: Antiangiogenic Effect Of Soy Isoflavonoidsmentioning

confidence: 99%

Soy and Breast Cancer: Focus on Angiogenesis

Varinská

Gál

Mojžišová

et al. 2015

IJMS

161

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“…Interestingly, several desmosomal genes have recently been linked to tumor suppressive activity (Chun and Hanahan, 2010, Dusek and Attardi, 2011), with the onset of cancer progression through methylation of desmosomal genes (Cui, et al, 2012a, Cui, et al, 2012b). Genistein has been shown to have anti-cancer effects through the inhibition of tyrosine kinases and the modulation of related cellular pathways (Mahmoud, et al, 2014, Nagaraju, et al, 2013). It is interesting to speculate that perhaps one of the many ways in which genistein acts to impede cancer progression is by affecting desmosomal adhesion through pathways similar to its protective effects in pemphigus models.…”

Section: Acquired Desmosomal Diseasesmentioning

confidence: 99%

Desmosomes in acquired disease

Stahley

Kowalczyk

2015

Cell Tissue Res

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Desmosomes are cell-cell junctions that mediate adhesion and couple the intermediate filament cytoskeleton to sites of cell-cell contact. This architectural arrangement functions to integrate adhesion and cytoskeletal elements of adjacent cells. The importance of this robust adhesion system is evident in numerous human diseases, both inherited and acquired, that occur when desmosome function is compromised. This review focuses on autoimmune and infectious diseases that impair desmosome function. In addition, we discuss emerging evidence that desmosomal genes are often misregulated in cancer. The emphasis of our discussion is placed on how human diseases inform our understanding of basic desmosome biology, and in turn, how fundamental advances in the cell biology of desmosomes may lead to new treatments for acquired diseases of the desmosome.

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“…Gen has multiple biological functions such as regulating lipid homeostasis and insulin resistance, counteracting inflammatory response, impeding cancer progression, alleviating Alzheimer's disease, and so on [17]. Accumulating evidence has shown that Gen can improve heart and blood vessel function and prevent cardiovascular diseases [18,19].…”

Section: Introductionmentioning

confidence: 99%

Genistein Protects H9c2 Cardiomyocytes against Chemical Hypoxia-Induced Injury via Inhibition of Apoptosis

Shi¹,

Zhang²,

Hu³

et al. 2019

Pharmacology

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Background/Aims: Hypoxia can induce cell injury in cardiomyocytes and further lead to cardiovascular diseases. Genistein (Gen), the predominant isoflavone found in soy products, has shown protective effects on cardiovascular system. The aim of the present study was to investigate the cardioprotective effect of Gen against chemical hypoxia-induced injury. Methods: Cobalt chloride (CoCl₂) was administrated to trigger chemical hypoxia in H9c2 cardiomyocytes. Cell proliferation was detected by using MTT assay. The expression level of hypoxia-related proteins (hypoxia-inducible factor [HIF]-1α and Notch-1) and apoptosis-related proteins (B cell lymphoma [Bcl]-2, Bax, and caspase-3) were evaluated by Western blot analysis. Results: In response to hypoxia, cell viability was reduced dramatically, whereas the expression of HIF-1α was upregulated. Hypoxia also induced cardiomyocytes apoptosis by reducing the ratio of Bcl-2/Bax and increasing expression of caspase-3. Interestingly, Gen attenuated CoCl₂-induced cell death and suppressed HIF-1α expression, as well as upregulated the expression of Notch-1. Furthermore, Gen could antagonize CoCl₂-induced apoptosis through upregulating Bcl-2/Bax ratio and inhibiting caspase-3 expression. Conclusions: Gen prevents chemical hypoxia-induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, exerting protective effects on H9c2 cardiomyocytes.

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Pleiotropic effects of genistein in metabolic, inflammatory, and malignant diseases

Cited by 73 publications

References 143 publications

Soy and Breast Cancer: Focus on Angiogenesis

Soy and Breast Cancer: Focus on Angiogenesis

Desmosomes in acquired disease

Genistein Protects H9c2 Cardiomyocytes against Chemical Hypoxia-Induced Injury via Inhibition of Apoptosis

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