Requirement of CLIC4 Expression in Human Colorectal Cancer Cells for Sensitivity to Growth Inhibition by Fucoxanthinol.

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.

• Authors: Reo Yokoyama, Ayumi Kushibiki, Shiori Yamada, Atsuhito Kubota, Hiroyuki Kojima, Tohru Ohta, Junichi Hamada, Hayato Maeda, Michihiro Mutoh, Masaru Terasaki
• Journal: Cancer genomics & proteomics (Cancer Genomics Proteomics) 2022 Jul-Aug Vol. 19 Issue 4 Pg. 428-444 ISSN: 1790-6245 [Electronic] Greece
• PMID: 35732323 (Publication Type: Journal Article)
• Copyright: Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Chemical References

• CLIC4 protein, human
• Chloride Channels
• beta Carotene
• fucoxanthinol

Topics

• Anoikis
• Cell Line, Tumor
• Chloride Channels (genetics)
• Colorectal Neoplasms (drug therapy, genetics, metabolism)
• Humans
• beta Carotene (analogs & derivatives, pharmacology)