卵巢癌细胞与巨噬细胞共培养对B7-H1表达的影响及机制

为了探讨卵巢癌细胞与巨噬细胞共培养后对B7．H1表达的影响及其可能机制，利用佛波酯（PMA）诱导THP-1或外周血单核细胞分化为巨噬细胞后，与人卵巢癌细胞株SKOV3体外非接触共培乔24h，qRT-PCR、Western blot以及流式细胞术分别检测SKOV3与巨噬细胞B7-H1的表达：进一步利用NF-KB、JAK2／STAT3、p38MAPK信号通路的抑制剂作用于共培养体系，检测B7-H1表达的变化，以探讨其机制。结果显示，共培养24h后，SKOV37L巨噬细胞B7-H1mRNA和蛋白的表达较非共培养组均显著升高（P〈0．05），而阻断NF-κB、JAK2／STAT3、p38MAPK信号通路后，B7-H1的上调均明显被抑制（P〈0．05）。SKOV3与巨噬细胞共培养后B7-H1的表达升高伊〈0．05），其机制可能涉及到NF—κB、JAK2／STAT3、p38MAPK信号通路的激活。

The Effects of Ovarian Cancer Cells Co-cultured with Macrophages on the Expression of B7-H1 and Its Mechanisms

To investigate the effects of ovarian cancer cells co-cultured with macrophages on the expression of B7-H1 and its possible mechanisms, phorbol 12-myristate 13-acetate （PMA） treated THP-1 cells or human monocytes were co-cultured with human ovarian cancer cell line SKOV3 for 24 h in vitro without direct contact, the expression of B7-H1 in SKOV3 cells and macrophages was detected by qRT-PCR, Western blot and flow cytometry, respectively; In addition, the expression of B7-H1 was also determined after treating the coculture system with inhibitors of NF-κB, JAK2/STAT3 or p38 MAPK signal pathways. These results suggested that the expression of BT-H1 was significantly elevated at both mRNA and protein levels in SKOV3 and macrophages after coculture for 24 h （P〈0.05）. However, the upregulation of B7-H1 expression was inhibited by blocking NF-κB, JAK2/STAT3 or p38 MAPK signal pathways （P〈0.05）. SKOV3 cells co-cultured with macrophages promoted the expression of B7-H1 （P〈0.05）, which was possible involved in the activation of NF-nB, JAK2/STAT3, p38 MAPK signal pathways.