Genistein-induced apoptosis and autophagocytosis in ovarian cancer cells

Gossner, Gabrielle; Choi, Milheon; Tan, Lijun; Fogoros, Sarah; Griffith, Kent A.; Kuenker, Megan; Liu, J. Rebecca

doi:10.1016/j.ygyno.2006.11.009

Cited by 150 publications

(82 citation statements)

References 43 publications

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“…This evidence suggests that genistein, which acts as an anticancer agent in combination with TRAIL, can be used to sensitize TRAIL-mediated apoptosis in TRAIL-resistant A549 cells. Some reports have shown that genistein induces autophagy and also initiates apoptosis in ovarian cancer cells (44). However, our results indicate that treatment with varying concentrations of genistein alone resulted in a dose-dependent increase in LC3-II and p62 levels in A549 adenocarcinoma cells.…”

Section: Discussioncontrasting

confidence: 75%

Genistein enhances TRAIL-induced cancer cell death via inactivation of autophagic flux

Nazim

Park

2015

Oncology Reports

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Abstract. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer agent as it selectively induces apoptosis in various types of tumor cells. Autophagic flux, which includes the complete process of autophagy, and suppression of autophagic flux has been increasingly recognized as a favorable and novel therapeutic approach for cancer treatment. Here, we showed that genistein, a major isoflavone compound that exerts its anticancer properties by inhibiting tumor cell proliferation, can induce TRAIL-mediated apoptotic cell death in TRAIL-resistant human adenocarcinoma A549 cells. Notably, genistein treatment led to a marked increase in the accumulation of microtubule-associated protein 1 light chain 3 (LC3)-II and p62 protein levels. The combination of genistein and TRAIL increased LC3-II, p62, activated caspase-3 and activated caspase-8 accumulation, confirming the inhibition of autophagic flux. Taken together, our results revealed that genistein enhanced TRAIL-induced tumor cell death in TRAIL-resistant A549 adenocarcinoma cells by inhibiting autophagic flux.

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Section: Discussioncontrasting

confidence: 75%

Genistein enhances TRAIL-induced cancer cell death via inactivation of autophagic flux

Nazim

Park

2015

Oncology Reports

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“…The effects of these diverse compounds will be discussed based on structural classification. and a caspase-independent cell death that exhibited hallmarks of autophagy (punctuate localization of LC3) and was accompanied by inhibition of Akt activation and glucose uptake (162). At doses of 25 and 50 Amol/L, again relatively high exposures compared with what occurs in humans eating considerable amounts of soy products, cytoplasmic vacuoles that stained positive for the autophagic marker monodansylcadaverine were detected.…”

Section: Such Findings Have Sparked Interest In Exploring the Importamentioning

confidence: 93%

Diet, Autophagy, and Cancer: A Review

Singletary

Milner

2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

146

102

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A host of dietary factors can influence various cellular processes and thereby potentially influence overall cancer risk and tumor behavior. In many cases, these factors suppress cancer by stimulating programmed cell death. However, death not only can follow the well-characterized type I apoptotic pathway but also can proceed by nonapoptotic modes such as type II (macroautophagy-related) and type III (necrosis) or combinations thereof. In contrast to apoptosis, the induction of macroautophagy may contribute to either the survival or death of cells in response to a stressor. This review highlights current knowledge and gaps in our understanding of the interactions among bioactive food constituents, autophagy, and cancer. Whereas a variety of food components including vitamin D, selenium, curcumin, resveratrol, and genistein have been shown to stimulate autophagy vacuolization, it is often difficult to determine if this is a protumorigenic or antitumorigenic response. Additional studies are needed to examine dose and duration of exposures and tissue specificity in response to bioactive food components in transgenic and knockout models to resolve the physiologic implications of early changes in the autophagy process. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1596 -610)

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“…In addition, genistein treatment also induces autophagic cell death in ovarian cancer cells, which may contribute to its potential to overcome chemoresistance developed from an altered apoptotic signaling pathway [20]. In both platinum-sensitive and platinum-resistant ovarian cancer cells, genistein abrogated NF-jB DNA binding activity and down-regulated anti-apoptotic genes [59].…”

Section: Genisteinmentioning

confidence: 99%

Modulation of inflammatory signaling pathways by phytochemicals in ovarian cancer

Kim

Han

et al. 2011

Genes Nutr

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Inflammation has been suggested to be involved in cancer development and progression. Many clinical and experimental studies have shown that inflammation could contribute to ovarian carcinogenesis through activation of the NF-jB and AP-1 pathways by chronic inflammatory mediators. Phytochemicals, which are natural compounds derived from fruits and vegetables, have shown anti-inflammatory and anti-cancer effects. Due to their relatively low toxicity and easy accessibility, phytochemicals have been investigated for their chemopreventive potential against various cancers. In this review, we discuss the role of phytochemicals in preventing ovarian cancer through anti-inflammatory mechanisms.

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Genistein-induced apoptosis and autophagocytosis in ovarian cancer cells

Cited by 150 publications

References 43 publications

Genistein enhances TRAIL-induced cancer cell death via inactivation of autophagic flux

Genistein enhances TRAIL-induced cancer cell death via inactivation of autophagic flux

Diet, Autophagy, and Cancer: A Review

Modulation of inflammatory signaling pathways by phytochemicals in ovarian cancer

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