[Effects of silencing inhibitor of DNA binding-1 gene on the growth and invasiveness of adenoid cystic carcinoma cells].

OBJECTIVE: To investigate the role of inhibitor of DNA binding-1 (Id-1) gene in adenoid cystic carcinoma cell growth and invasion behavior. METHODS: With salivary adenoid cystic carcinoma cell lines ACC-M and ACC-2, dedected Id-1 gene expression was screened with immunofluorescence assay. After Id-1 mRNA knocking-down using small interfering RNA, RT-PCR and Western blot were used to detect the different expressions before and after interference, and the growth of cells before and after interference was deceted using the MTT assay, and the cell invasion ability was checked with the use of Transwell chamber assay. RESULTS: Id-1 were both expressed in the ACC-M and ACC-2, and the expression in ACC-M was higher than that in ACC-2. After Id-1 RNA interference, the growth and invasiveness of ACC-M and ACC-2 were inhibited with the restrained degree in ACC-M much stronger than that in the ACC-2. CONCLUSION: In view of the important role of Id-1 in the behavior of growth and invasion in ACC cell, interfering the expression of Id-1 gene is expected to be a novel and effective means for the treatment of adenoid cystic carcinoma.

The action of a novel fluoroquinolone antibiotic agent antofloxacin hydrochloride on human-ether-à-go-go-related gene potassium channel.

The administration of certain fluoroquinolone antibacterials has recently been linked to QT interval prolongation, raising the clinical concerns over the cardiotoxicity of these agents. In this study, the effects of a novel fluoroquinolone, antofloxacin hydrochloride (AX) on human-ether-à-go-go-related gene (HERG) encoding potassium channels and the biophysical mechanisms of drug action were performed with whole-cell patch-clamp technique in transiently transfected HEK293 cells. The administration of AX caused voltage- and time-dependent inhibition of HERG K+ current (I(HERG/MiRP1)) in a concentration-dependent manner but did not markedly modify the properties of channel kinetics, including activation, inactivation, deactivation and recovery from inactivation as well. In comparison with sparfloxacin (SPX), levofloxacin lactate (LVFX), the potency of AX to inhibit HERG tail currents was the least one, with an IC(50) value of 460.37 microM. By contrast, SPX was the most potent compound, displaying an IC(50) value of 2.69 microM whereas LVFX showed modest potency, with an IC(50) value of 43.86 microM, respectively. Taken together, our data suggest that AX only causes a minor reduction of I(HERG/MiRP1) at the estimated free plasma level.