Furthermore, biochemical assays illustrated that rs3750050 could impair the inhibitory effect of PTPN12 on Ras/MEK/ERK signaling by impeding SHC dephosphorylation, increase the expression of cyclin D1 and ultimately lead to aberrant cell proliferation, thus contributing to CRC pathogenesis.
MiR-519d negatively regulated the expression of CCND1 via directly bound to CCND1 3`UTR. si-CCND1 could downregulate the CCND1 expression in colorectal cancer HCT116 and SW480 cells. si-CCND1 increased the sensitivity of colorectal cancer cells to 5-Fu.
Cyclin D1, CDK4 and Ras were revealed to be expressed significantly higher in poorly differentiated CRC compared with moderately differentiated CRC (P<0.05).
Phenylethynyl-substituted Heterocycles Inhibit Cyclin D1 and Induce the Expression of Cyclin-dependent Kinase Inhibitor p21<sup>Wif1/Cip1</sup> in Colorectal Cancer Cells.
Tumor and adjacent healthy tissues were obtained from 100 patients diagnosed with CRC. miR-466 expression was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). mRNA and protein levels of cyclin D1, apoptosis regulator BAX (BAX), and matrix metalloproteinase-2 (MMP-2) were analyzed by qRT-PCR and Western blot, respectively, in SW-620 CRC cells transfected with miR-466 mimics or negative control miRNA.
We found that compared with GG homozygote genetic model, AA, AG, AA + AG genetic models of the CCND1G870A polymorphism were significantly associated with overall CRC risk (AA homozygote genetic model: OR = 1.28, 95% CI = 1.10-1.49; AG heterozygote genetic model: OR = 1.15, 95% CI = 1.06-1.25; AA homozygote + AG heterozygote genetic model: OR = 1.19, 95% CI = 1.07-1.33).
The DEGs may function in CRC by interacting with other genes in the PPI network of the top 50 nodes, for example, DEP domain‑containing MTOR‑interacting protein (DEPTOR)‑CCND1, AURKA‑breast carcinoma amplified sequence‑1 (BCAS1), CCND1‑BCAS1, CCND1‑neural precursor cell expressed developmentally downregulated 9 (NEDD9) and CCND1‑mitogen‑activated protein kinase kinase 2 (MAP2K2).
The present study was designated to clarify whether common single nucleotide polymorphisms (SNPs) of the transcription factor 7- like 2 (TCF7L2) and cyclin D1 (CCND1) genes are associated with colorectal cancer risk in Mexican patients.
These findings support the concept that the cell cycle regulation may play a role in colorectal cancer initiation and development and CCND1A870G genotyping maybe a feasible technology for colorectal cancer early detection.
The quantitative level of the β-catenin protein was significantly decreased in the CRC cell lysates, hence the expression level of c-Myc and cyclin D1 was significantly decreased following 2.5mM CaLa treatment.
In addition, to better understand the role of CCND1 and CDH1 in the pathophysiology of CRC, the expression pattern was evaluated in analogous tumor and adjacent normal tissues from 23 CRC patients by Western blot analysis.
There was no significantly reduced risk of CRC by CHRT or ERT use, however a reduced risk of T-stage 1-2 tumours was seen among CHRT users (HR: 0.24; 95% CI: 0.09-0.77).Analysis stratified by tumour location revealed a reduced overall risk of rectal, but not colon, cancer among CHRT and ERT users, including T stage 1-2, lymph node negative, distant metastasis-free, cyclin D1 - and p53 negative tumours.In unadjusted analysis, OC use was significantly associated with a reduced overall risk of CRC (HR: 0.56; 95% CI: 0.44-0.71), but this significance was not retained in adjusted analysis (HR: 1.05: 95% CI: 0.80-1.37).