Study Of The C-fos Gene In Adenoid Cystic Carcinoma-2Cells Induced By Arsenic Trioxide

Objective To investigate the inhibition mechanism of arsenic trioxide(As2O3) by observing the growth and apoptosis-inducing effects on adenoid cystic carcinoma-2(ACC-2) cells in vitro,and provide the theoretical basis for the clinical application of As2O3by detecting the c-fos gene expression of ACC-2.Methods (1)Different concertration of As2O3were applied to ACC-2cells for different time and the morphology of ACC-2cells was observed under inverted phase contrast microscope;(2) RT-PCR was applied to investegate the expression of c-fos mRNA level in ACC-2cells after treated with different concertration of As2O3for different time;(3)The expression of c-fos protein was observed by immunohistochemical after As2O3treatment. Using SPSS17.0statistical analysis package to carry on the data processing, inspection level for a=0.05.Results(1)As2O3can inhibit the proliferation of ACC-2cells and induce apoptosis;(2)The results of RT-PCR show that the c-fos mRNA get a high expression in ACC-2cells,and the c-fos mRNA expression was obviously suppressed with the time and As2O3concertration increasing as a time-and dose-dependenty correlation pattern. C-fos gene expressed lowest-volume in6μmol/L concertration at48h, the data has a statistically significant (P=0.00).(3)Immunohistochemistry revealed that the expression of c-fos protein is localized in nuclei stained with brown-yellow or brown, and with no staining in plasma. C-fos protein is highly expressed in ACC-2cells,its expression decresed after ACC-2cells treated with As2O3in a time-and dose-dependent manner with significantly difference(P=0.00).Conclusion (1)As2O3might markedly depressed the growth of ACC-2cells in vitro and induce the cell apoptosis;(2) As2O3could suppress the expression of c-fos gene and protein, and this effect is in a time-and dose-dependent manner;(3) c-fos gene may play a significant role on ACC-2cell apoptosis induced by As2O3, the study provides certain theoretical basis for clinical application by further discusses molecular mechanism of As2O3on ACC.