Western blot or qRT-PCR was used to analyze the effect of NEK2 on the phosphorylation levels of ERK and c-JUN in two GC cell lines (BGC823 and SGC7901) with NEK2 overexpression, and the expression of the downstream effector cyclin D1.
Utilizing MTT, clonogenic, flow cytometry, wound healing and Transwell invasion assays in addition to Western blotting, the present study demonstrated that the overexpression of T-cad suppressed GC cell growth and colony formation via cell cycle arrest at the G0/G1 phase via downregulating the expression of cyclin dependent kinase 4 and Cyclin D1.
This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.
Upregulation of miR-143 inhibited cell proliferation, invasion, S phase cell proportion and cell cycle related protein levels of Cyclin D1, CDK4 and CDK6 in GC.
When stratifying by the type, Sex and H. pylori infection in dominant model, Interestingly, we found the opposite result in Male (AA + GA vs. GG: OR=0.5, 95% CI=0.33-0.76, P=0.001), there were no association between CCND1G870A polymorphism and GC risk in any other subgroup.
The Kaplan-Meier method and cox proportional hazards model were used to analyze the relationship of HOXA1 and cyclin D1 expression with GC clinical outcomes.
The Significant Role of Cyclin D1 in the Synergistic Growth-inhibitory Effect of Combined Therapy of Vandetanib with 5-Fluorouracil for Gastric Cancer.
Fz2 shRNA suppressed cell proliferation and motility of MKN45 and MKN74 cells, and downregulated cyclin D1 and MMP-9 expression in these GC cell lines.
Overall, 78% of GC cases harbored one clinically relevant GA or more, with the most frequent alterations being found in TP53 (50%), ARID1A (24%), KRAS (16%), CDH1 (15%), CDKN2A (14%), CCND1 (9.5%), ERBB2 (8.5%), PIK3CA (8.6%), MLL2 (6.9%), FGFR2 (6.0%), and MET (6.0%).
Since overexpressed cyclin D1 is closely related to human gastric cancer progression, inhibition of cyclin D1 using specific targeting could be an effective treatment method of human gastric cancer.
Furthermore, β-cryptoxanthin induced an accumulation of cells in the G1/G0 phase of the cell cycle (as detected by flow cytometry), which was in accordance with an increased expression of p21 and down regulations of cyclin D1 and cyclin E, detected by Western blot analysis, and β-cryptoxanthin increased the mRNA levels of retinoic acid receptor β (RARβ) with the treatment at 10 μM for 24 h. Collectively, the above findings suggest that β-cryptoxanthin could be therapeutic in the treatment of stomach cancer cell in vitro.
These data indicate that miR-9 suppresses the expression of cyclin D1 and Ets1 via the binding sites in their 3'-UTR, thus inhibiting the proliferation, invasion and metastasis of gastric cancer.
Genetic polymorphism of CCND1 is associated with CIHM status in gastric cancer, especially in the advanced stage, but is independent of clinico-pathological features.
CCND1 genotype distribution among the patients was significantly different from that among controls; AA (odds ratio (OR)=0.348, 95% CI: 0.163-0.742) and GA (OR=0.715, 95% CI: 0.506-1.012) genotypes were significantly lower in the gastric cancer patients than in the controls when subjects with the GG genotype served as the reference category.
The data suggested that URG4 played an important role in the development of human gastric cancer by regulating the expression of cyclin D1 and might be used as a potential therapeutic target for gastric cancer.