Licochalcone A-Induced Human Bladder Cancer T24 Cells Apoptosis Triggered by Mitochondria Dysfunction and Endoplasmic Reticulum Stress

Xuan, Yue; Li, Defang; Zhao, Hong; Jiang, Jiangtao; Wang, Penglong; Ma, Xiaoyi; Sun, Xiling; Zheng, Qi

doi:10.1155/2013/474272

Cited by 40 publications

(41 citation statements)

References 38 publications

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“…These results agree with a previous report in which LicA inhibited proliferation, increased levels of ROS, and induced apoptosis in T24 cells [98]. This compound also induced mitochondrial dysfunction, caspase-3 activation, and PARP cleavage and caused endoplasmic reticulum (ER) stress-dependent apoptosis [98].…”

Section: Antioxidant Effectssupporting

confidence: 93%

“…Evidence suggested that LicA inhibited proliferation by increasing the levels of intracellular ROS because the affects could be attenuated by treatment with the glutathione precursor and antioxidant, N-acetyl-cysteine (NAC) [97]. These results agree with a previous report in which LicA inhibited proliferation, increased levels of ROS, and induced apoptosis in T24 cells [98]. This compound also induced mitochondrial dysfunction, caspase-3 activation, and PARP cleavage and caused endoplasmic reticulum (ER) stress-dependent apoptosis [98].…”

Section: Antioxidant Effectssupporting

confidence: 91%

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Chemopreventive Effects of Licorice and Its Components

Bode

Dong

2015

Curr Pharmacol Rep

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Section: Antioxidant Effectssupporting

confidence: 93%

Section: Antioxidant Effectssupporting

confidence: 91%

Chemopreventive Effects of Licorice and Its Components

Bode

Dong

2015

Curr Pharmacol Rep

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“…Licochalcone-A, a chalconoid and a type of natural phenol, has been isolated from the root of the licorice plant and has exhibited various pharmacological effects, including antimalarial, anticancer, antibacterial and antiviral properties (7). Furthermore, treatment with licochalcone-A induced apoptosis in various cancer cell types, including oral (36), bladder (37,38), lung (39), gastric (40) and prostate cancer cells (41). In addition, Lico-E, a retrochalone, with various pharmacological effects, including antiparasitic, antibacterial, antioxidative and superoxide-scavenging properties, has been isolated from the root of licorice (24).…”

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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“…Furthermore, it has been reported that LCA induces apoptosis in HepG2 hepatocellular carcinoma cells through induction of ER stress via a phospholipase C gamma 1-, Ca 2+ -and ROS-dependent pathway (22). Our previous studies have demonstrated that LCA may significantly increase ROS levels and induce apoptosis of T24 human bladder cancer cells (23). However, the underlying molecular mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 96%

Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels

Yang

Jiang

Yang

et al. 2016

Molecular Medicine Reports

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Abstract. Licochalcone A (LCA) has been reported to significantly inhibit cell proliferation, increase reactive oxygen species (ROS) levels, and induce apoptosis of T24 human bladder cancer cells via mitochondria and endoplasmic reticulum (ER) stress-triggered signaling pathways. Based on these findings, the present study aimed to investigate the mechanisms by which LCA induces apoptosis of T24 cells. Cultured T24 cells were treated with LCA, and cell viability was measured using the sulforhodamine B assay. Apoptosis was detected by flow cytometry with Annexin V/propidium iodide staining, and by fluorescent microscopy with Hoechst 33258 staining. The levels of intracellular free calcium ions were determined using Fluo-3 AM dye marker. Intracellular ROS levels were assessed using the 2' ,7'-dichlorodihydrofluorescein diacetate probe assay. The mitochondrial membrane potential was measured using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl benzimidazole carbocyanine iodide. Furthermore, the mRNA expression levels of B-cell lymphoma (Bcl)-extra large, Bcl-2-associated X protein, Bcl-2-interacting mediator of cell death, apoptotic protease activating factor-1 (Apaf-1), calpain 2, cysteinyl aspartate specific proteinase (caspase)-3, caspase-4 and caspase-9 were determined using reverse transcription semiquantitative and quantitative polymerase chain reaction analyses. Treatment with LCA inhibited proliferation and induced apoptosis of T24 cells, and increased intracellular Ca 2+ levels and ROS production. Furthermore, LCA induced mitochondrial dysfunction, decreased mitochondrial membrane potential, and increased the mRNA expression levels of Apaf-1, caspase-9 and caspase-3. Exposure of T24 cells to LCA also triggered calpain 2 and caspase-4 activation, resulting in apoptosis. These findings indicated that LCA increased intracellular Ca 2+ levels, which may be associated with mitochondrial dysfunction. In addition, the ER stress pathway may be considered an important mechanism by which LCA induces apoptosis of T24 bladder cancer cells. IntroductionNatural herbal medicines have long been used to treat cancer. Biomedical research and cancer treatment clinical trials have provided evidence regarding the use of herbal medicines; therefore, they are increasingly being accepted as a complementary and alternative treatment (1). In addition, natural medicines have been reported to have an important role in human health, particularly certain well-studied plants, including Taxus chinensis (Taxus madia) (2), Radix Sophorae flavescentis (Sophora flavescens) (3), Alkanna tinctoria, Lithospermum erythrorhizon and licorice (Glycyrrhiza L) (4). Licorice is one of the most commonly prescribed herbs in Chinese Traditional Medicine, and has been used for >2,000 years. The effects of licorice have been reported on various diseases, ranging from microbial infection to cancer (5-7). However, since herbs usually contain numerous chemical compositions, the mechanism of action of these herbs is currently unclear. Recently, several chemical ing...

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Licochalcone A-Induced Human Bladder Cancer T24 Cells Apoptosis Triggered by Mitochondria Dysfunction and Endoplasmic Reticulum Stress

Cited by 40 publications

References 38 publications

Chemopreventive Effects of Licorice and Its Components

Chemopreventive Effects of Licorice and Its Components

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

Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels

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