The effects of genistein and daidzein on cell proliferation kinetics in HT29 colon cancer cells: the expression of CTNNBIP1 (β-catenin), APC (adenomatous polyposis coli) and BIRC5 (survivin)

Lepri, Sandra Regina; Zanelatto, Leonardo Campos; Silva, Patrícia Benites Gonçalves da; Sartori, Daniele; Ribeiro, Lúcia Regina; Mantovani, Mário Sérgio

doi:10.1007/s13577-012-0051-6

Cited by 30 publications

(15 citation statements)

References 30 publications

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“…Oral administration of genistein also inhibited angiogenesis and suppressed metastasis of colorectal cancer to distant organs in mice [133]. According to in vitro studies, the anticancer effects of genistein on colorectal cancer might involve the suppression of Wnt, NF-κB signaling pathways [134,135]. Additionally, in nude mice inoculated with liver cancer cells, oral administration of genistein (50 mg/kg/day) significantly suppressed the intrahepatic metastasis [136].…”

Section: Experimental Studiesmentioning

confidence: 99%

Natural Polyphenols for Prevention and Treatment of Cancer

et al. 2016

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There is much epidemiological evidence that a diet rich in fruits and vegetables could lower the risk of certain cancers. The effect has been attributed, in part, to natural polyphenols. Besides, numerous studies have demonstrated that natural polyphenols could be used for the prevention and treatment of cancer. Potential mechanisms included antioxidant, anti-inflammation as well as the modulation of multiple molecular events involved in carcinogenesis. The current review summarized the anticancer efficacy of major polyphenol classes (flavonoids, phenolic acids, lignans and stilbenes) and discussed the potential mechanisms of action, which were based on epidemiological, in vitro, in vivo and clinical studies within the past five years.

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Section: Experimental Studiesmentioning

confidence: 99%

Natural Polyphenols for Prevention and Treatment of Cancer

et al. 2016

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“…It has been found that blocking the HIF-1α pathway by inhibitors such as genistein [41,42] and YC-1 [43,44] results in the down-regulation of survivin expression in tumor cells, diminishing angiogenesis and tumor growth. Genistein exhibited a similar effect in the present study, in which HIF-1α-mediated survivin expression under hypoxic conditions and HIF-1α inhibition by genistein in HUVECs led to reduced rather than completely diminished survivin expression, even in the presence of 200 μM of genistein, implying that hypoxiainduced survivin expression can be initiated through other molecular pathways besides HIF-1α.…”

Section: Discussionmentioning

confidence: 99%

The Effect and Mechanism of Celecoxib in Hypoxia-Induced Survivin Up-Regulation in HUVECs

Liu

Zhao

Cai

2015

Cell Physiol Biochem

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Background/Aims: To investigate the roles of hypoxia-inducible factor 1α (HIF-1α), cyclooxygenase-2 (Cox-2) and its product, Prostaglandin E2 (PGE₂), in the mechanisms underlying hypoxia-induced survivin expression in human umbilical vein endothelial cells (HUVECs) and to examine the effect of celecoxib, a selective Cox-2 inhibitor, on survivin expression. Methods: HUVECs were exposed to a normal (95% O₂) or hypoxic (3% O₂) environment for 24 hrs. We observed the localized expression of survivin, Cox-2 and HIF-1α in HUVECs using immunocytochemistry and detected the inhibitory effects of celecoxib on the growth of HUVECs using an MTT assay. mRNA and protein levels of Cox-2, HIF-1α and survivin were determined by real-time PCR and Western blot analysis under hypoxic conditions for 0, 6, 12, or 24 hrs. The time course changes of HIF-1α and survivin protein expression induced by cobalt chloride (CoCl₂) were studied using Western blot analysis. We then treated HUVECs under hypoxia for 24 hrs with celecoxib (a Cox-2 selective inhibitor), genistein (a HIF-1α inhibitor) or exogenous PGE₂ to further investigate the changes in hypoxia-induced survivin expression. Results: Following 24 hrs of hypoxic treatment, cells exhibited strongly positive survivin, HIF-1α and Cox-2 cytoplasmic staining. Celecoxib (65 μM) effectively inhibited cell proliferation under hypoxic conditions. The protein and mRNA levels of Cox-2, HIF-1α and survivin were increased under hypoxia. The patterns of HIF-1α and survivin expression induced by CoCl₂ were similar to those induced by exposure to hypoxia. Genistein partially blocked survivin expression. Celecoxib reversed the hypoxia-induced survivin expression, whereas the addition of PGE₂ partially restored this effect. Conclusions: Hypoxia-induced survivin expression in HUVECs may be mediated by dual interdependent mechanisms directly involving HIF-1α and indirectly involving the Cox-2/PGE₂ pathways. Celecoxib may offset hypoxia-induced survivin expression.

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“…A number of studies suggest that soy isoflavones, mainly genistein, may suppress growth of different cancer cells including breast cancer cells (Chen and Chien 2014;Choi and Kim 2013;Lepri et al 2014;Mukherjee et al 2010). As it was mentioned above genistein displays structural similarities with estradiol and may act as an agonist or antagonist of ER.…”

Section: In Vitro Studiesmentioning

confidence: 99%

Critical Dietary Factors in Cancer Chemoprevention

Ullah¹,

Ahmad²

2016

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The effects of genistein and daidzein on cell proliferation kinetics in HT29 colon cancer cells: the expression of CTNNBIP1 (β-catenin), APC (adenomatous polyposis coli) and BIRC5 (survivin)

Cited by 30 publications

References 30 publications

Natural Polyphenols for Prevention and Treatment of Cancer

Natural Polyphenols for Prevention and Treatment of Cancer

The Effect and Mechanism of Celecoxib in Hypoxia-Induced Survivin Up-Regulation in HUVECs

Critical Dietary Factors in Cancer Chemoprevention

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