Induction of Apoptosis by the Licochalcone E in Endothelial Cells via Modulation of NF-.KAPPA.B and Bcl-2 Family

Chang, Hee J.; Yoon, Goo; Park, Jung Sun; Kim, Mi Ha; Baek, Min Kyung; Kim, Nam Ho; Shin, Boo Ahn; Ahn, Bong Whan; Cheon, Seung Hoon; Jung, Young Do

doi:10.1248/bpb.30.2290

Cited by 44 publications

(23 citation statements)

References 17 publications

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“…Chang et al (42) have reported that Lico-E induced cell death in ECV 302 cells, which are an immortalized human umbilical vein endothelial cell line. However, in the present study, Lico-E did not affect the cytotoxicity of the primary cultured hNOKs, whereas cytotoxicity was increased in the FaDu cells treated with Lico-E.…”

Section: Discussionmentioning

confidence: 99%

Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells through the extrinsic and intrinsic apoptotic signaling pathways

Cho

Kang

et al. 2017

Oncology Letters

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Abstract. The aim of the present study was to investigate licochalcone-E (Lico-E)-induced apoptosis and the associated apoptotic signaling pathway in FaDu cells, a human pharyngeal squamous carcinoma cell line. Treatment with Lico-E exhibited significant cytotoxicity on FaDu cells in a concentration-dependent manner. The IC 50 value of Lico-E in FaDu cells was ~50 µM. Treatment with Lico-E increased the number of dead FaDu cells. Furthermore, chromatin condensation, which is associated with apoptotic cell death, was observed in FaDu cells treated with Lico-E for 24 h. By contrast, Lico-E did not produce cytotoxicity or increase the number of dead cells when applied to human normal oral keratinocytes (hNOKs). Furthermore, chromatin condensation was not observed in hNOKs treated with Lico-E. Treatment with Lico-E increased the expression of Fas ligand and the cleaved form of caspase-8 in FaDu cells. Furthermore, treatment with Lico-E increased the expression of pro-apoptotic factors, including apoptosis regulator BAX, Bcl-2-associated agonist of cell death, apoptotic protease-activating factor 1, caspase-9 and tumor suppressor p53, while decreasing the expression of anti-apoptotic factors, including apoptosis regulator Bcl-2 and Bcl-2-like protein 1 in FaDu cells. The expression of cleaved caspases-3 and poly (ADP-ribose) polymerase was significantly upregulated following treatment with Lico-E in FaDu cells, while Lico-E-induced apoptotic FaDu cell death was partially suppressed by treatment with Z-VAD-FMK, a pan caspase inhibitor. Therefore, Lico-E-induced oral cancer (OC) cell-specific apoptosis is mediated by the death receptor-dependent extrinsic and mitochondrial-dependent intrinsic apoptotic signaling pathways. In conclusion, these data suggested that Lico-E exhibits potential chemopreventive effects and warrants further developed as a chemotherapeutic agent against OC.

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Section: Discussionmentioning

confidence: 99%

Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells through the extrinsic and intrinsic apoptotic signaling pathways

Cho

Kang

et al. 2017

Oncology Letters

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Section: Licochalcone Ementioning

confidence: 91%

“…LicE suppressed ECV304 bladder epithelial-like cell growth and induced apoptosis [113]. Similarly to LicA, LicE inhibited activation of NF-κB and was associated with a change in the Bax/Bcl-2 ratio that favored apoptosis [113]. BALB/c mice were injected with 4T1 mammary carcinoma cells into the mammary fat pads and then 7 days later, were administered LicE (7 or 14 mg/kg BW/day) orally for 25 days [114].…”

Section: Licochalcone Ementioning

confidence: 99%

Chemopreventive Effects of Licorice and Its Components

Bode

Dong

2015

Curr Pharmacol Rep

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“…The cells transfected with RON siRNA showed a clear decrease in the DNA-binding activity of NF-κB and in the protein level of the p65 subunit of NF-κB in nuclear lysates. The involvement of NF-κB in the apoptotic response of the RON siRNA transfected gastric cancer cells was suggested based on the following: i) The known target genes of NF-κB include a number of anti-apoptotic genes such as the Bcl-2 family (19), ii) NF-κB activity is important to cell survival (20), and iii) the inactivation of the endogenous Rel/NF-κB factors by suppressor forms of the inhibitory protein, IκΒ·, sensitizes the cells to stimulus-induced apoptosis (21).…”

Section: Discussionmentioning

confidence: 99%

Small interfering RNA targeting of Recepteur d'Origine Nantais induces apoptosis via modulation of nuclear factor-κB and Bcl-2 family in gastric cancer cells

Park¹,

Lee²,

Joο³

et al. 2010

Oncol Rep

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Abstract.The abnormal accumulation and activation of the receptor tyrosine kinase, Recepteur d'Origine Nantais (RON), has been implicated in tumorigenesis and metastasis in epithelial tumors including gastric cancer. This study examined whether the sequence-specific small interfering RNA (siRNA) suppression of the RON expression could induce apoptotic cell death, and investigated the involved molecular mechanisms. Sequence-specific siRNA effectively suppressed the RON expression at both the mRNA and protein levels. Silencing of the RON expression significantly inhibited gastric cancer cell proliferation and induced apoptosis in a time-dependent manner. The induction of apoptosis was confirmed by the ladder-patterned DNA fragmentation, the presence of cleaved and condensed nuclear chromatin and the increased number of annexin V-positive cells. RONtargeted siRNA effectively inhibited the constitutive nuclear factor-κB (NF-κB) activation as revealed by an altered electrophoretic mobility shift. In agreement with this, silencing of the RON expression resulted in a decrease in the nuclear level of the p65 subunit of NF-κB. The transfection of siRNA, which blocked the RON expression, also caused a change in the ratio of Bax/Bcl-2 in a manner that favored apoptosis. The siRNA silencing of RON induced cytochrome c release and the activation of caspase-8 and caspase-9. These results indicate that RON-targeted siRNA could be therapeutically efficacious by inducing cell apoptosis through the modulation of the NF-κB and Bcl-2 family in gastric cancer cells.

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Induction of Apoptosis by the Licochalcone E in Endothelial Cells via Modulation of NF-.KAPPA.B and Bcl-2 Family

Cited by 44 publications

References 17 publications

Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells through the extrinsic and intrinsic apoptotic signaling pathways

Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells through the extrinsic and intrinsic apoptotic signaling pathways

Chemopreventive Effects of Licorice and Its Components

Small interfering RNA targeting of Recepteur d'Origine Nantais induces apoptosis via modulation of nuclear factor-κB and Bcl-2 family in gastric cancer cells

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