An amplification/overexpression of the CCND1 gene plays an important role in the enhancement of cell transformation in esophageal squamous cell carcinoma cells.
CDK4/6 inhibitor-SHR6390 exerted potential antitumor activity against ESCC cell lines and xenografts, and evaluation of CDK6 and Cyclin D1 expressions might be helpful to select patients beneficial from SHR6390, which provided evidences for future clinical trials.
Determination of the cyclin D1 (G870A) single nucleotide polymorphism may be suitable to identify individuals with increased risk for ESCC or CAC in the northern Chinese population.
DNA ploidy pattern, Ki-67 labeling index (LI), and cyclin D1 and p53 protein expression were examined and detailed pathologic examinations were conducted on tumors from 53 patients (46 males and 7 females with a mean age of 66 years [range, 47-85 years]) with surgically resected esophageal squamous cell carcinoma and the prognostic value of these factors was evaluated.
Downregulation of HDAC2 expression evidently inhibited cell proliferation, arrested cell cycle at the G0/G1 phase and induced cell apoptosis in ESCC EC9706 cells, coupled with increased expression of p21 and Bax proteins and decreased expression of cyclin D1 and Bcl-2 proteins.
Finally, the stable transfection of RRIG1 inhibited esophageal SCC cell growth and the expression of extracellular signal-regulated protein kinases 1 and 2 and cell cycle-related genes (e.g., cyclin D1, phosphorylated Rb, and E2F).
Further investigation in the effect of miR-503 on ESCC cell proliferation, migration, and invasion showed that enhanced expression of miR-503 inhibited ESCC aggressive phenotype and overexpression of CCND1 reversed the effect of miR-503-mediated ESCC cell aggressive phenotype.
Here we identify that Wnt2/beta-catenin signaling pathway is activated in ESCC cells, and sodium nitroprusside (SNP) and siRNA against beta-catenin not only inhibit the expressions of beta-catenin and its major downstream effectors including c-myc and cyclin D1, but induce cell cycle arrest and apoptosis, suggesting that Wnt2/beta-catenin pathway may be a potential molecular target for ESCC therapy.
Here we report that entinostat reversed cisplatin resistance in ESCC both in vitro and in vivo by induction of apoptosis and inhibition of cell proliferation, accompanied by a decrease of multidrug resistance gene 1 (MDR1), P-Src, Mcl-1, Cyclin D1 and an increase of cleaved PARP.
Human ESCC cell line EC109 was cultured with aspirin and cigarette smoke extract (CSE) at different concentrations for 48 h. Cell growth was tested with 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide reduction assay; cyclin D(1) mRNA level was detected by reverse transcription-polymerase chain reaction assays; protein level of cyclin D(1) was detected by Western blot; the cell cycle change was monitored by flow cytometry detection assays.
In conclusion, LCM coupled with real-time fluorescence quantitative-PCR technique is more precise than PCR for the identifying amplified oncogenes; The role of CCND1 amplification in ESCC development and progression needs more extensive study.
In situ hybridization and immunohistochemistry were used respectively to detect the expression of mRNA and proteins of Egr-1, c-fos and cyclin D1 in 70 cases of esophageal squamous cell carcinoma and their corresponding para-cancerous mucosa and upper cut edge mucosa.
In this study, we investigated the expression pattern of beta-catenin and cyclin D1 using immunohistochemistry and searched for mutations in exon 3 of the beta-catenin gene and Axin gene in esophageal squamous cell carcinoma.