Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0154059 (
Esophagus
)
2,950
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The relationship between smoking and esophageal squamous cell carcinoma (ESCC) has been confirmed by epidemiology. Cyclin D(1) plays a critical role in regulating the cell cycle; it is an important regulator of cell cycle and can function as a transcriptional co-regulator. The importance of
cyclin D
(1) makes it an attractive target for anticancer therapy. 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. CSE stimulated cell proliferation, increased the protein level of
cyclin D
(1) in a dose-dependent manner (P < 0.01), and decreased the proportion of G(0)/G(1) phase cell of cell cycle. However, aspirin can inhibit the cell growth and suppress the protein level of
cyclin D
(1) after CSE affected the EC109 cell line in a dose-dependent manner (P < 0.01). Meanwhile, aspirin increased the proportion of G(0)/G(1) phase cell, while that of S and G(2)/M phases decreased. Aspirin can inhibit the cell growth and suppress the protein level of
cyclin D
(1) after CSE affected EC109 cell line. The probable mechanism is through decreasing the expression of
cyclin D
(1), thus stopping the transition of cell cycle from G(0)/G(1) to S phase.
Dis
Esophagus
2009
PMID:Influence of aspirin and cigarette smoke extract on the expression of cyclin D1 and effects of cell cycle in esophageal squamous cell carcinoma cell line. 1920 49