›› 2009, Vol. 29 ›› Issue (10): 1187-.

• Original article (Basic research) • Previous Articles     Next Articles

Arsenic trioxide induced JAK/STAT3 pathway inhibition in myeloma cell lines

WANG Ming-ming, ZOU Li-fang, DOU Hong-ju, ZHU Qi, REN Zhi-hong, HU Jun-pei   

  1. Department of Hematology, The Ninth People's Hospital, Shanghai Institute of Hematology, School of Medicine, Shanghai Jiaotong University, Shanghai 200011, China
  • Online:2009-10-25 Published:2009-10-26
  • Supported by:

    Shanghai Jiaotong University School of Medicine Foundation, 05XJ21023


Objective To explore the possible relationship between alteration of cell cycle and JAK/STAT3 signal transduction pathway inhibition induced by arsenic trioxide (As2O3) in myeloma cell lines U266 and RPMI8226 in vitro. Methods Multiple myeloma cell lines U266 and RPMI8226 were used as in vitro models. The influence of As2O3 on myeloma cells were evaluated by MTT assay and flow cytometry. Meanwhile, methylation specific PCR and Western blotting were employed to detect the methylation status of gene SOCS-1 and protein expression level of P-STAT3 in these cells after As2O3 treatment. Results As2O3 significantly inhibited the growth of U266 and RPMI8226 cells in a dose-dependent manner. Furthermore, cell cycle was arrested at G0/G1 phase with inhibition of protein expression level of P-STAT3 and SOCS-1 gene demethylation after exposure to As2O3 for 72 h(r=0.85, P<0.05). Conclusion As2O3 could induce the alteration of cell cycle which might be related to JAK/STAT3 signal transduction pathway inhibition and SOCS-1 demethylation in myeloma cell lines. The study puts forward a new idea of As2O3 treatment in multiple myeloma.

Key words: arsenic trioxide, myeloma, SOCS-1, JAK/STAT3, cell cycle

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