细胞粘附介导的耐药（CAM-DR）是多发性骨髓瘤不可治愈的重要原因。抗凋亡是CAM-DR发生的重要原因。凋亡抑制蛋白PEA15与细胞的凋亡耐受有密切关系。信号转导与转录激活因子1（STAT1）可以通过调节凋亡信号分子的表达在调控肿瘤细胞耐药过程中发挥重要作用。前期研究发现，miR-217、PEA15、STAT1均与CAM-DR相关，miR-217可靶向抑制PEA15的表达，并且PEA15可以与STAT1相互作用。因此推测：miR-217可能通过调节PEA15继而影响STAT1及其下游凋亡信号分子的表达参与CAM-DR进程。课题组拟分析PEA15、miR-217对PEA15的调节以及PEA15与STAT1的相互作用的调节机制在CAM-DR进程中的作用；然后全面分析miR-217对PEA15的调节在STAT1介导的CAM-DR进程中的意义，从而进一步揭示CAM-DR的机制。

Cell adhesion-mediated drug resistance is an important reason for the incurability of multiple myeloma. Anti-apoptosis is the vital reason in the process of CAM-DR. PEA15, an anti-apoptotic protein, is closely correlated with cell apoptosis. It is reported that STAT1 has a vital role in the regulation of drug resistance by regulating the expression of apoptosis-related protein. Our research group has recently identified that miR217, PEA15 and STAT1 were all associated with CAM-DR. Furthermore, we found that PEA15 was a target gene of miR-217 and PEA15 could interact with STAT1. Therefore, we speculate that miR-217 may be involved in regulation of STAT1 and its apoptotic target genes via targeting PEA15, and thereby participating in CAM-DR. Based on these, we first aim to analyze the role of PEA15 in CAM-DR. Then, we intend to explore the effect of miR-217 on the expression of PEA15 and CAM-DR. Subsequently, we will investigate the regulatory mechanism of PEA15-STAT1 interaction and its effect on CAM-DR phenotype. Finally, we will comprehensively analyze the significance of PEA15-STAT1 interaction in the process of STAT1-mediated CAM-DR phenotype. Our research will shed new light on the mechanism of CAM-DR and provide theoretical basis for clinical treatment of multiple myeloma.