Browsing by Author "Lin, Chien-I"

Now showing 1 - 4 of 4

Combination of Aurora A and Haspin inhibitors enhances p53 expression and tumor growth inhibition in human colorectal cancer
(2016-04-01)
Chang, Yun-Hsuan
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Lin, Chien-I
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Chen, Zan-Chu
;
Liu, Kuang-Kai
;
Chao, Jui-I
Combination of Aurora A and Haspin inhibitors enhances p53 expression and tumor growth inhibition in human colorectal cancer
(2016-04-01)
Chang, Yun-Hsuan
;
Lin, Chien-I
;
Chen, Zan-Chu
;
Liu, Kuang-Kai
;
Chao, Jui-I
Expression of Survivin and p53 Modulates Honokiol-Induced Apoptosis in Colorectal Cancer Cells
(2014-11-01)
Lai, Ying-Jiun
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Lin, Chien-I
;
Wang, Chia-Lin
;
Chao, Jui-I
;
交大名義發表
Honokiol is a small biphenolic compound, which exerts antitumor activities; however, the precise mechanism of honokiol-induced apoptosis in the human colorectal cancer cells remains unclear. Here, we show that survivin and p53 display the opposite role on the regulation of honokiol-induced apoptosis in the human colorectal cancer cells. Honokiol induced the cell death and apoptosis in various colorectal cancer cell lines. Moreover, honokiol elicited the extrinsic death receptor pathway of DR5 and caspase 8 and the intrinsic pathway of caspase 9. The common intrinsic and extrinsic downstream targets of activated caspase 3 and PARP protein cleavage were induced by honokiol. Interestingly, honokiol reduced anti-apoptotic survivin protein and gene expression. Transfection with a green fluorescent protein (GFP)-survivin-expressed vector increased the colorectal cancer cell viability and resisted the honokiol-induced apoptosis. Meantime, honokiol increased total p53 and the phosphorylated p53 proteins at Ser15 and Ser46. The p53-wild type colorectal cancer cells were exhibited greater cytotoxicity, apoptosis and survivin reduction than the p53-null cancer cells after treatment with honokiol. Together, these findings demonstrate that the existence of survivin and p53 can modulate the honokiol-induced apoptosis in the human colorectal cancer cells. J. Cell. Biochem. 115: 1888-1899, 2014. (c) 2014 Wiley Periodicals, Inc.
The depletion of securin enhances butein-induced apoptosis and tumor inhibition in human colorectal cancer
(2014-09-05)
Huang, Yu-Tin
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Lin, Chien-I
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Chien, Pei-Hsuan
;
Tang, Tsai-Tai
;
Lin, Johnson
Butein (3,4,2\',4\'-tetrahydroxychalcone) is a promising natural polyphenolic compound that shows the growth inhibitory activity in human cancer cells; however, the precise mechanism is still unclear. Securin plays pivotal role in cancer cell proliferation and tumorigenesis. Here, we report the presence of securin that could modulate apoptosis and tumor growth ability in the butein-treated human colorectal cancer. Butein induced caspase-3 activation and PARP protein cleavage for apoptosis induction in human colorectal cancer cells. Interestingly, butein reduced the securin protein levels but conversely increased the phospho-histone H3 proteins, mitotic arrest and abnormal chromosomes segregation in cancer cells. The securin-null colorectal cancer cells were more sensitive on the reduction of cell viability than the securin-wild type cancer cells following butein treatment. The loss of securin in human colorectal cancer cells decreased tumor growth ability in nude mice. Moreover, butein reduced the tumor size of xenografted human colorectal tumors of nude mice. Taken together, this study demonstrates for the first time that the depletion of securin mediates the butein-induced apoptosis and colorectal tumor inhibition. (C) 2014 Elsevier Ireland Ltd. All rights reserved.