Abstract
Purpose : To investigate the antitumor effect of candidone extracted from Derris indica , against human cholangiocarcinoma (CCA) cells. Methods : Candidone was purified from the hexane extract of Derris indica fruit. CCA cell lines, KKUM156 and KKU-M213, were treated with candidone. Sulforhodamine B (SRB) assay and acridine orange/ethidium bromide (AO/EB) staining were used to investigate the effects of candidone on cell proliferation and induction of apoptosis, respectively. The effect on cell migration was assessed by wound healing assay. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was employed to assess the effects of candidone on the expression of genes that regulate proliferation and apoptosis. Results : Candidone exerted strong anticancer effects on CCA cells. The agent suppressed CCA cell proliferation and induced apoptotic cell death. RT-qPCR assay revealed that candidone significantly increased the expression of anti-proliferative and pro-apoptotic genes, including p21 and Bax, and decreased the expression of anti-apoptotic genes, including Bcl-2 and survivin. Moreover, candidone inhibited the migration of CCA cells induced by IGF-1. Conclusion : Candidone exhibits potent antitumor effect on CCA cells. These findings suggest that candidone is potentially suitable for the management of CCA and, therefore, warrants further investigation. Keywords : Candidone, Derris indica, Cholangiocarcinoma, Cytotoxicity, Apoptosis
Highlights
The incidence of cholangiocarcinoma (CCA) is increasing worldwide [1]
To determine the efficacy of candidone (Figure 1) in CCA cells, two CCA cell lines; KKU-M156 and KKU-M213 were exposed to various concentrations from 0.5 - 10 μg/mL for 8 and 24 h
Since candidone mediated antiproliferation in CCA cells, we determined whether candidone can induce apoptosis in CCA cells
Summary
The incidence of cholangiocarcinoma (CCA) is increasing worldwide [1]. Phytochemicals with bio-active properties, including antioxidant and antitumor effects, have been widely studied. These may shed some light on potential candidates in preclinical study of anticancer agents [6]. Many phytochemicals have been shown to suppress cellular signaling pathways and promote cancer cell death. They behave like pro-oxidants, increasing oxidative stress in cancer cells by inhibiting ROS scavenging system, inactivating pro-survival signaling pathways, and triggering apoptotic cell death [7]. Bioflavonoids are a large group of bioactive compounds that mediate antitumor effects in many cancer models. In CCA, luteolin suppresses the proliferation and migration of CCA cell lines [9]
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