Chayanit Piyawajanusorn1,2, Yingpinyapat Kittirat1,2, Prakasit Sa-Ngiamwibool2,3, Attapol Titapun2,4, Watcharin Loilome1,2, Nisana Namwat5,2. 1. Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 2. Cholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, Khon Kaen, Thailand. 3. Department of Pathology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 4. Department of Surgery, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 5. Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand nisana@kku.ac.th.
Abstract
BACKGROUND/AIM: This study examined the in vitro effects of the bile duct cancer drug PRIMA-1MET on cholangiocarcinoma (CCA) cell growth to determine its potential usefulness in CCA therapy. MATERIALS AND METHODS: The effect of this drug on the expression of senescent markers (p16INK4A and p21) and the phosphorylation of p53 was investigated, as was the association between senescent markers and the patients' clinicopathological data. RESULTS: PRIMA-1MET inhibited CCA cell growth with the half maximal-inhibitory concentration (IC50) values of 21.9-40.8 μM. PRIMA-1MET induced phospho-p53, p16INK4A and p21 triggering cellular senescence and apoptosis. High expressions of p16INK4A and p21 were associated with a high survival rate of patients with CCA. CONCLUSION: PRIMA-1MET may potentially be an alternative anticancer agent that might lead to a better prognosis in patients with CCA. Copyright
BACKGROUND/AIM: This study examined the in vitro effects of the bile duct cancer drug PRIMA-1MET on cholangiocarcinoma (CCA) cell growth to determine its potential usefulness in CCA therapy. MATERIALS AND METHODS: The effect of this drug on the expression of senescent markers (p16INK4A and p21) and the phosphorylation of p53 was investigated, as was the association between senescent markers and the patients' clinicopathological data. RESULTS: PRIMA-1MET inhibited CCA cell growth with the half maximal-inhibitory concentration (IC50) values of 21.9-40.8 μM. PRIMA-1MET induced phospho-p53, p16INK4A and p21 triggering cellular senescence and apoptosis. High expressions of p16INK4A and p21 were associated with a high survival rate of patients with CCA. CONCLUSION: PRIMA-1MET may potentially be an alternative anticancer agent that might lead to a better prognosis in patients with CCA. Copyright
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