Proliferation inhibition effect of indomethacin on CML cells associated with down-regulation of phosphorylated STAT1/STAT5 and inhibition of COX-2 expression].

Guang-sen Zhang, Yun-bi Fu, Meng Xia

Institute of Molecular Hematology, the Second Xiangya Hospital, Central South University, Changsha 410011, China.

Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 2004 Dec

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To explore the mechanism of anti-proliferative effect of indomethacin (IN) on chronic myelogenous leukemia (CML) cells. MTT was applied to assay CML cells viability under IN intervention. STAT1, STAT5 proteins were analyzed by Western blot, the expressions of phosphorylated STAT1 or STAT5 by immunoprecipitation combined with Western blot, the cellular localization of p-STATs proteins by indirect immunofluorescence technique, and the detection of Bcl-X(L) and COX-2 protein by Western blot. IN could significantly inhibit the viability of CML cells. 0 approximately 400 micromol/L of IN could down-regulate the expression of p-STAT1 or p-STAT5 in a dose-response manner, p-STATs were distributed mainly in the nucleus as scattering spots. The expression of COX-2 protein could be detected in K562 cells. Both Bcl-X(L) and COX-2 proteins could be inhibited by IN in a dose-dependent manner. IN could significantly inhibit the proliferation of CML cells, the mechanism of which might be related to the suppression of STATs/Bcl-X(L) signal transduction pathway. There exists COX-2 protein expression in K562 cells, the anti-leukemia effect of IN was possibly dependent on COX-2 pathway.

Citation

Guang-sen Zhang, Yun-bi Fu, Meng Xia. Proliferation inhibition effect of indomethacin on CML cells associated with down-regulation of phosphorylated STAT1/STAT5 and inhibition of COX-2 expression]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi. 2004 Dec;25(12):732-5