Tu1829 The Effects of Ursodeoxycholic Acid on Cell Cycle, Reactive Oxygen Species, and Proliferation of Colon Cancer Cell

Kim, Su Young; Kim, Eunkyoung; Jeong, Arong; Kim, Yoon Jae; Kim, Eui Joo; Cho, Jae Hee; Park, Dong Kyun; Kwon, Kwang An; Chung, Jun‐Won; Kim, Kyoung Oh

doi:10.1016/s0016-5085(16)33223-1

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“…ROS are a by-product of the aerobic metabolism of organisms ( 21 ). It has previously been demonstrated that active oxygen is closely associated with tumor formation, cell cycle and apoptosis ( 22 ). To detect whether UDCA could induce increased intracellular ROS levels in M14 cells, the intracellular ROS level was examined using flow cytometry ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…UDCA is able to improve a series of biochemical and histological parameters (prothrombin time, alkaline phosphatase, alanine transaminase, fatigue, hepatomegaly or splenomegaly) induced by primary biliary cirrhosis, thereby prolonging the patient's survival ( 29 ). It has previously been reported that UDCA could effectively induce apoptosis in liver cancer, gastric cancer and colon cancer cell lines ( 7 , 30 – 32 ). However, to the best of our knowledge the role of UDCA in human melanoma has not yet been explored.…”

Section: Discussionmentioning

confidence: 99%

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Apoptosis induced by ursodeoxycholic acid in human melanoma cells through the mitochondrial pathway

Huang

et al. 2018

Oncol Rep

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Ursodeoxycholic acid (UDCA) is a type of hydrophilic bile acid extracted from animal bile with a wide range of biological functions. The present results demonstrated that UDCA could effectively inhibit the proliferation of two human melanoma cell line (M14 and A375) with time- and concentration-dependence. Following exposure to various concentrations of UDCA, M14 cells exhibited typical morphological changes and weaker ability of colony forming. Flow cytometry analysis demonstrated that UDCA could induce a decrease of mitochondrial membrane potential and an increase in reactive oxygen species (ROS) levels in M14 cells. The cell cycle was arrested in the G2/M phase, which was confirmed by the decrease of cyclin-dependent kinase 1 and cyclinB1 at the protein level. However, when M14 cells were treated with UDCA and Z-VAD-FMK (caspase inhibitor) synchronously, the apoptosis rate of the cells was reduced significantly. In addition, it was demonstrated that UDCA induced apoptosis of human melanoma M14 cells through the ROS-triggered mitochondrial-associated pathway, which was indicated by the increased expression of cleaved-caspase-3, cleaved-caspase-9, apoptotic protease activating factor-1, cleaved-poly (ADP-ribose) polymerase 1 and the elevation of B cell lymphoma-2 (Bcl-2) associated X protein/Bcl-2 ratio associated with apoptosis. Therefore, UDCA may be a potential drug for the treatment of human melanoma.

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Section: Resultsmentioning

confidence: 99%