Reo Yokoyama1, Ayumi Kushibiki1, Shiori Yamada1, Atsuhito Kubota1, Hiroyuki Kojima1,2, Tohru Ohta2, Junichi Hamada2,3, Hayato Maeda4, Michihiro Mutoh5, Masaru Terasaki6,2. 1. School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan. 2. Advanced Research Promotion Center, Health Sciences University of Hokkaido, Hokkaido, Japan. 3. School of Nursing and Social Services, Health Sciences University of Hokkaido, Hokkaido, Japan. 4. Faculty of Agriculture and Life Science, Hirosaki University, Aomori, Japan. 5. Department of Molecular-Targeting Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. 6. School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan; terasaki@hoku-iryo-u.ac.jp.
Abstract
BACKGROUND/AIM: Fucoxanthinol (FxOH), a marine carotenoid, induces apoptosis and anoikis in human colorectal cancer (CRC) DLD-1 cells via the down-regulation of chloride intracellular channel 4 (CLIC4) expression, a key molecule for apoptosis. However, whether FxOH is susceptible to CLIC4 expression and its regulatory mechanisms in human CRC cells remains unknown. We investigated the inhibitory effects of FxOH on six types of human CRC cells with CLIC4 regulation. MATERIALS AND METHODS: The association between FxOH and CLIC4 was investigated using gene knockdown, overexpression, and transcriptome analyses. RESULTS: CLIC4 expression in CRC cells was a significant factor associated with sensitivity to FxOH. CLIC4 regulates many cancer-related signals and participates in growth inhibition in FxOH-treated DLD-1 cells. Both CLIC4 knockdown and overexpression attenuated the inhibitory effects of FxOH on DLD-1 cells. CONCLUSION: Our findings suggest that the protein expression of CLIC4 and its regulating mechanisms play significant roles regarding cell death in human CRC cells by FxOH treatment. Further investigation by in vitro and in vivo models is needed to determine the effect of CLIC4.
BACKGROUND/AIM: Fucoxanthinol (FxOH), a marine carotenoid, induces apoptosis and anoikis in human colorectal cancer (CRC) DLD-1 cells via the down-regulation of chloride intracellular channel 4 (CLIC4) expression, a key molecule for apoptosis. However, whether FxOH is susceptible to CLIC4 expression and its regulatory mechanisms in human CRC cells remains unknown. We investigated the inhibitory effects of FxOH on six types of human CRC cells with CLIC4 regulation. MATERIALS AND METHODS: The association between FxOH and CLIC4 was investigated using gene knockdown, overexpression, and transcriptome analyses. RESULTS: CLIC4 expression in CRC cells was a significant factor associated with sensitivity to FxOH. CLIC4 regulates many cancer-related signals and participates in growth inhibition in FxOH-treated DLD-1 cells. Both CLIC4 knockdown and overexpression attenuated the inhibitory effects of FxOH on DLD-1 cells. CONCLUSION: Our findings suggest that the protein expression of CLIC4 and its regulating mechanisms play significant roles regarding cell death in human CRC cells by FxOH treatment. Further investigation by in vitro and in vivo models is needed to determine the effect of CLIC4.
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