Cytotoxic effects of dimethyl-celecoxib (DMC) on bone tumor cell line MG63 and cell line HEK293

Abstract Dimethyl-celecoxib (DMC), is a celecoxib (CXB) derivative has no inhibitory function on cyclooxygenase-2 (COX-2) and displays antitumor properties. This substance can be helpful in advancing the treatment of COX-2-indipentent cancers. In the current study, we assayed the efficacy of DMC on MG63 bone tumor cell line and Human embryonic kidney (HEK293) cell line. The cellular viability, nitrogen monoxide content, and Inducible nitric oxide synthases (iNOS) gene expression were measured respectively with MTT (The MTT assay is a colorimetric assay for assessing cell metabolic activity.) Griess reaction, and real-time Reverse transcription polymerase chain reaction (RT-PCR) procedures .IC50 was determined by MTT assay, and iNOS gene expression was evaluated by RT-PCR. Also, monoxide nitrogen production was monitored by a Griess test and finally one-way Anova (Analysis of Variance (ANOVA) is a statistical formula used to compare variances across the means (or average) of different groups.) and T-test were used to analyze the data. Results showed that Dimethylcelloxib at concentrations of: 62.5, 125, 250, 500 µg /ml at 48 h significantly decreased the survival rate of MG63 and HEK293 tumor cells (P < 0.001). It was found that iNOS gene expression decreased significantly (P < 0.001) and production of monoxide nitrogen molecule had a significant increase (P < 0.01 and P < 0.001). since Dimethylceloxib reduced iNOS gene expression, it was expected to decrease nitrogen monoxide, but this drug showed its cytotoxic effects through increased nitrogen monoxide production.