Angelicin potentiates <scp>TRAIL</scp>‐induced apoptosis in renal carcinoma <scp>C</scp>aki cells through activation of caspase 3 and down‐regulation of c‐<scp>FLIP</scp> expression

Min, Kyoung‐jin; Um, Hee Jung; Seo, Seung Un; Woo, Seon Min; Kim, Shin; Park, Jong‐Wook; Lee, Hyun‐Shik; Kim, Sang Hyun; Choi, Yung Hyun; Lee, Tae-Jin; Kwon, Taeg Kyu

doi:10.1002/ddr.21414

Cited by 28 publications

(9 citation statements)

References 22 publications

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“…Angelicin increases Bax, caspase-3, -9, decreases Bcl-2, Bcl-xL, Mcl-1 in A549 (NSCLC) cells [33], and SH-SY5Y cells [59] to induce intrinsic mitochondria-mediated apoptosis. Angelicin, and in combination, activated caspase-3 and decreased FADD like IL-1β converting enzyme inhibitory protein (c-FLIP) in Caki (renal carcinoma) cells to induce apoptosis [60]. Bergamottin induces apoptosis in human colon carcinoma cell line (RKO) and HT-29 cells by increasing caspase-3, 8, and 9; and PARP cleavage [61].…”

Section: Pi3k/akt Inhibitionmentioning

confidence: 99%

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Ahmed

Khan

Aschner

et al. 2020

IJMS

128

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Cancer is one of the most extreme medical conditions in both developing and developed countries around the world, causing millions of deaths each year. Chemotherapy and/or radiotherapy are key for treatment approaches, but both have numerous adverse health effects. Furthermore, the resistance of cancerous cells to anticancer medication leads to treatment failure. The rising burden of cancer overall requires novel efficacious treatment modalities. Natural medications offer feasible alternative options against malignancy in contrast to western medication. Furanocoumarins’ defensive and restorative impacts have been observed in leukemia, glioma, breast, lung, renal, liver, colon, cervical, ovarian, and prostate malignancies. Experimental findings have shown that furanocoumarins activate multiple signaling pathways, leading to apoptosis, autophagy, antioxidant, antimetastatic, and cell cycle arrest in malignant cells. Additionally, furanocoumarins have been shown to have chemo preventive and chemotherapeutic synergistic potential when used in combination with other anticancer drugs. Here, we address different pathways which are activated by furanocoumarins and their therapeutic efficacy in various tumors. Ideally, this review will trigger interest in furanocoumarins and their potential efficacy and safety as a cancer lessening agents.

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Section: Pi3k/akt Inhibitionmentioning

confidence: 99%

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Ahmed

Khan

Aschner

et al. 2020

IJMS

128

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“…Interestingly, the pro-apoptotic protein Bim was shown to increase in its expression when Caki cells which were only treated with angelicin; however, combination treatment with TRAIL attenuated the effect. The combination treatment of angelicin and TRAIL was able to induce apoptosis in other cancer cell lines, such as Sk-hep1 and MDA-MB-361 cells but normal cell lines were not affected (Min et al, 2018). This is a good therapeutic option to be exploited as this combination treatment could have the potential to be used as targeted cancer therapy toward cancer cell lines that are resistant to TRAIL.…”

Section: North America and Chinamentioning

confidence: 99%

“…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). Further investigation then went on to show how this combination treatment was even more effective than cycloheximide in downregulating cellular FLICE (FADD-like IL-1b-converting enzyme)-inhibiting protein (c-FLIP) posttranslationally.…”

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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“…Notably, non-small cell lung cancer cell lines such as A549, H1299, and H596 cells are known to be resistant to TRAIL-induced apoptosis [ 6 ]. Recently, several groups reported the synergistic or additive effect of phytochemicals, such as kaempferol [ 7 ], angelicin [ 8 ], and curcumin [ 9 ], on TRAIL-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Lambertianic Acid Sensitizes Non-Small Cell Lung Cancers to TRAIL-Induced Apoptosis via Inhibition of XIAP/NF-κB and Activation of Caspases and Death Receptor 4

Ahn

Lee

Hwang

et al. 2018

IJMS

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Lambertianic acid (LA) is a biologically active compound from the leaves of Pinus koraiensis. In the present study, apoptotic mechanisms of LA plus TNF-related apoptosis-inducing ligand (TRAIL) were elucidated in non-small cell lung cancer cells (NSCLCs). Cytotoxicity assay, flow cytometry, immunoprecipitation, and Western blotting were performed. Here, combined treatment of LA and TRAIL increased cytotoxicity, sub-G1 population, cleaved poly (ADP-ribose) polymerase (PARP), and caspase3/8/9 in A549 and H1299 cells compared to LA or TRAIL alone. Furthermore, combined treatment of LA and TRAIL significantly decreased antiapoptotic proteins such as B-cell lymphoma 2 (Bcl-2), Fas-like inhibitor protein (FLIP), and X-linked inhibitor of apoptosis protein (XIAP), and enhanced the activation of proapoptotic proteins Bid compared to LA or TRAIL alone. In addition, combined treatment of LA and TRAIL upregulated the expression of Death receptor 4 (DR4) and downregulated phosphorylation of nuclear factor κ-light-chain-enhancer of activated B cells (p-NF-κB), inhibitory protein of kB family (p-IκB), and FLIP in A549 and H1299 cells along with disrupted binding of XIAP with caspase3 or NF-κB. Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.

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Angelicin potentiates TRAIL‐induced apoptosis in renal carcinoma Caki cells through activation of caspase 3 and down‐regulation of c‐FLIP expression

Cited by 28 publications

References 22 publications

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Angelicin—A Furocoumarin Compound With Vast Biological Potential

Lambertianic Acid Sensitizes Non-Small Cell Lung Cancers to TRAIL-Induced Apoptosis via Inhibition of XIAP/NF-κB and Activation of Caspases and Death Receptor 4

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