Publication: 3,3'-diindolylmethane downregulates cyclin D1 through triggering endoplasmic reticulum stress in colorectal cancer cells
Issued Date
2017-01-01
Resource Type
ISSN
17912431
1021335X
1021335X
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2-s2.0-85020769145
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Mahidol University
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SCOPUS
Bibliographic Citation
Oncology Reports. Vol.38, No.1 (2017), 569-574
Suggested Citation
Xiaobo Zhang, Pakin Sukamporn, Shiqiang Zhang, Kyung Won Min, Seung Joon Baek 3,3'-diindolylmethane downregulates cyclin D1 through triggering endoplasmic reticulum stress in colorectal cancer cells. Oncology Reports. Vol.38, No.1 (2017), 569-574. doi:10.3892/or.2017.5693 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/42093
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Title
3,3'-diindolylmethane downregulates cyclin D1 through triggering endoplasmic reticulum stress in colorectal cancer cells
Abstract
As a major in vivo condensation product of indole-3-carbinol, which is mostly present in cruciferous vegetables, 3,3'-diindolylmethane (DIM) has been previously reported with anti-proliferative action in different types of cancer by our group and others. To further elucidate these underlying mechanisms, we examined the effect of DIM on cyclin D1, which was aberrantly overexpressed in various cancer cells and tumors. Herein, we found that DIM downregulated cyclin D1 expression in colorectal cancer cells (CRC), which was independent of PPAR-expression and protease activity. Furthermore, DIM did not affect cyclin D1 mRNA expression, suggesting DIM modulated cyclin D1 expression at the translational level. Subsequently, blocking eIF2-phosphorylation resulted from endoplasmic reticulum (ER) stress restored cyclin D1 in the presence of DIM. Thus, the present study demonstrates that DIM downregulates cyclin D1 through triggering ER stress in human colorectal cancer cells.