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The Mechanism of IL-12 for the Differentiation and Apoptosis of Acute Mononuclear Leukemia Cells
Wu Bitao, Ma Tingting, Lin Yan, Xiong Haiyu, Wang Qin, Cheng Feng, Li Ziwei, Tu Zhiguang*
Key Laboratory of Laboratory Medical Diagnostics of Education Ministry, College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China
Abstract: As we all know， interleukin-12 (IL-12) plays a critical role in anti-tumor responses. Our previous morphological and functional study has revealed that over-expression of IL-12 would induce monocytic leukemia cell differentiation. In this study， we examined the differentiation markers， changes of cell proliferation， cell cycle and apoptosis in THP-1 cells after IL-12 treatment to investigate its likely mechanism for the differentiation and apoptosis of acute mononuclear leukemia cells. It was found that the macrophage surface marker CD68 and CD11b mRNA and protein expression increased in a time-dependent manner， and CD68+ and CD11b+ positive cells significantly increased. Furthermore， IL-12-induced THP-1 cell differentiation was accompanied by the G1 or G1/S phase growth arrest with G1 phase cells accumulation and S phase cells reduction. Cell apoptosis rate increased significantly， especially the early apoptosis cells; anti-apoptosis protein Bcl-2 was down-expressed， and pro-apoptosis protein Fas was up-regulated. These findings have revealed that IL-12 is likely to play a role of anti-tumor on acute mononuclear leukemia through inducing monocytic tumor cells differentiation to mature macrophages， suppressing tumor cells malignant proliferation and increasing tumor cells apoptosis.
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