In:
Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Computers, Materials and Continua (Tech Science Press), Vol. 27, No. 7 ( 2019-07-12), p. 739-750
Abstract:
The activated form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], regulates numerous cellular processes, including inhibition of cancer progression. IL-1β has been reported to facilitate cancer development, especially by inducing an epithelial-to-mesenchymal transition (EMT) in several malignant tumors. However, the underlying mechanism of 1,25(OH)2D3 and IL-1β in colorectal cancer (CRC) still remains largely unknown. To fill in this knowledge gap, we measured cell proliferation and invasion by CCK-8 and Transwell assays after stimulation with 1,25(OH)2D3
and IL-1β. E-cadherin and vimentin were chosen as markers of EMT measured by immunofluorescence, quantitative real-time PCR (qRT-PCR), and Western blot. The expression and function of the vitamin D receptor (VDR) was evaluated by Western blot and luciferase reporter assay. qRT-PCR and RNA-FISH were performed to detect the expression and location of lncTCF7 in vitro. The binding sites of VDR in the lncTCF7 promoter were confirmed by a chromatin immunoprecipitation assay. Based on the above experiments, we found that 1,25(OH)2D3 attenuates IL-1β-induced increased proliferation
and invasion in colorectal cancer through enhancing VDR, which inhibits the expression of lncTCF7 by directly binding to its promoter region.
Type of Medium:
Online Resource
ISSN:
0965-0407
DOI:
10.3727/096504018X15360541345000
Language:
English
Publisher:
Computers, Materials and Continua (Tech Science Press)
Publication Date:
2019
detail.hit.zdb_id:
1114699-0
detail.hit.zdb_id:
2044620-2
