Galangin sensitizes TRAIL-induced apoptosis through down-regulation of anti-apoptotic proteins in renal carcinoma Caki cells

Han, Min Ae; Lee, Dong Hee; Woo, Seon Min; Seo, Bo Ram; Min, Kyoung‐jin; Kim, Shin; Park, Jong‐Wook; Kim, Sang Hyun; Choi, Yung Hyun; Kwon, Taeg Kyu

doi:10.1038/srep18642

Cited by 28 publications

(18 citation statements)

References 28 publications

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“…Galangin, a flavonoid extracted from the root of Alpinia officinarum was reported to possess antiproliferative action and to inhibit renal cell carcinoma (786-0 and Caki-1) invasion by suppressing EMT, inducing apoptosis and producing ROS in renal carcinoma cells (Cao et al, 2016 ). Han et al ( 2016 ) observed that the combination of galangin and TRAIL significantly induced apoptosis in renal carcinoma (Caki, ACHN, and A498) but not in normal mouse kidney cells or human normal mesangial cells, suggesting the potential utilization of galangin as a sensitizer of TRAIL-resistant cancer cell therapy. Meng et al ( 2015 ) combined quercetin with anti-sense oligo gene therapy (Snail gene inhibition) and found that each suppressed the proliferation and migration of Caki-2 cells, inducing cell cycle arrest and apoptosis, with a strong suppression of renal carcinoma cells being achieved by their combination.…”

Section: Renal Carcinomamentioning

confidence: 99%

Flavonoids in Kidney Health and Disease

et al. 2018

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This review summarizes the latest advances in knowledge on the effects of flavonoids on renal function in health and disease. Flavonoids have antihypertensive, antidiabetic, and antiinflammatory effects, among other therapeutic activities. Many of them also exert renoprotective actions that may be of interest in diseases such as glomerulonephritis, diabetic nephropathy, and chemically-induced kidney insufficiency. They affect several renal factors that promote diuresis and natriuresis, which may contribute to their well-known antihypertensive effect. Flavonoids prevent or attenuate the renal injury associated with arterial hypertension, both by decreasing blood pressure and by acting directly on the renal parenchyma. These outcomes derive from their interference with multiple signaling pathways known to produce renal injury and are independent of their blood pressure-lowering effects. Oral administration of flavonoids prevents or ameliorates adverse effects on the kidney of elevated fructose consumption, high fat diet, and types I and 2 diabetes. These compounds attenuate the hyperglycemia-disrupted renal endothelial barrier function, urinary microalbumin excretion, and glomerular hyperfiltration that results from a reduction of podocyte injury, a determinant factor for albuminuria in diabetic nephropathy. Several flavonoids have shown renal protective effects against many nephrotoxic agents that frequently cause acute kidney injury (AKI) or chronic kidney disease (CKD), such as LPS, gentamycin, alcohol, nicotine, lead or cadmium. Flavonoids also improve cisplatin- or methotrexate-induced renal damage, demonstrating important actions in chemotherapy, anticancer and renoprotective effects. A beneficial prophylactic effect of flavonoids has been also observed against AKI induced by surgical procedures such as ischemia/reperfusion (I/R) or cardiopulmonary bypass. In several murine models of CKD, impaired kidney function was significantly improved by the administration of flavonoids from different sources, alone or in combination with stem cells. In humans, cocoa flavanols were found to have vasculoprotective effects in patients on hemodialysis. Moreover, flavonoids develop antitumor activity against renal carcinoma cells with no toxic effects on normal cells, suggesting a potential therapeutic role in patients with renal carcinoma.

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Section: Renal Carcinomamentioning

confidence: 99%

Flavonoids in Kidney Health and Disease

et al. 2018

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“…On the contrary, human renal carcinoma (Caki) cells displayed a different kind of result when incubated with angelicin. Caki cells have always been known to be one of those cancer cell lines that are resistant to tumor necrosis factor (TNF) apoptosis inducing ligand (TRAIL) (Han et al, 2016). When the compound was tested alone, angelicin was not able to induce apoptosis, yet when incubated together with 50 ng/ml of TRAIL the combined treatment was able to promote cell death (Min et al, 2018).…”

Section: North America and Chinamentioning

confidence: 99%

Angelicin—A Furocoumarin Compound With Vast Biological Potential

et al. 2020

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Angelicin, a member of the furocoumarin group, is related to psoralen which is well known for its effectiveness in phototherapy. The furocoumarins as a group have been studied since the 1950s but only recently has angelicin begun to come into its own as the subject of several biological studies. Angelicin has demonstrated anti-cancer properties against multiple cell lines, exerting effects via both the intrinsic and extrinsic apoptotic pathways, and also demonstrated an ability to inhibit tubulin polymerization to a higher degree than psoralen. Besides that, angelicin too demonstrated anti-inflammatory activity in inflammatory-related respiratory and neurodegenerative ailments via the activation of NF-kB pathway. Angelicin also showed pro-osteogenesis and pro-chondrogenic effects on osteoblasts and pre-chondrocytes respectively. The elevated expression of proosteogenic and chondrogenic markers and activation of TGF-b/BMP, Wnt/b-catenin pathway confirms the positive effect of angelicin bone remodeling. Angelicin also increased the expression of estrogen receptor alpha (ERa) in osteogenesis. Other bioactivities, such as anti-viral and erythroid differentiating properties of angelicin, were also reported by several researchers with the latter even displaying an even greater aptitude as compared to the commonly prescribed drug, hydroxyurea, which is currently on the market. Apart from that, recently, a new application for angelicin against periodontitis had been studied, where reduction of bone loss was indirectly caused by its anti-microbial properties. All in all, angelicin appears to be a promising compound for further studies especially on its mechanism and application in therapies for a multitude of

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“…However, a lot of cancer cells reveal resistance to TRAIL through multiple mechanisms, including down-regulation of death receptor (DR)4/5, and up-regulation of decoy death receptors and anti-apoptotic proteins [ 12 , 13 , 14 ]. New approaches to overcome TRAIL resistance that combined treatment with pharmacological agents that modify the function of tumor-dysregulated apoptotic genes have been investigated [ 15 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Garcinol Enhances TRAIL-Induced Apoptotic Cell Death through Up-Regulation of DR5 and Down-Regulation of c-FLIP Expression

et al. 2018

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Garcinol is a polyisoprenylated benzophenone derived from the Garcinia indica fruit that possess potential therapeutic effects such as inhibition of inflammation and tumor expansion. Here, we investigated whether garcinol induces TRAIL sensitization in renal carcinoma cells. Single treatment with garcinol or TRAIL did not effect on apoptosis. However, combined treatment with garcinol plus TRAIL significantly induced apoptosis in renal carcinoma (Caki, ACHN and A498), lung carcinoma (A549), and hepatoma (SK-Hep1) cells. In contrast, garcinol plus TRAIL did not alter cell viability in normal cells. Garcinol plus TRAIL induced up-regulation of DR5 and down-regulation of c-FLIP expression at post-translational levels. Furthermore, knock-down of DR5 by siRNA and ectopic expression of c-FLIP blocked apoptotic cell death induced by garcinol plus TRAIL. Overall, our study provides evidence that garcinol can be exploited as a potential TRAIL sensitizer.

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Galangin sensitizes TRAIL-induced apoptosis through down-regulation of anti-apoptotic proteins in renal carcinoma Caki cells

Cited by 28 publications

References 28 publications

Flavonoids in Kidney Health and Disease

Flavonoids in Kidney Health and Disease

Angelicin—A Furocoumarin Compound With Vast Biological Potential

Garcinol Enhances TRAIL-Induced Apoptotic Cell Death through Up-Regulation of DR5 and Down-Regulation of c-FLIP Expression

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