Wnt5b是非经典Wnt信号通路中的配体，它能够与Fz受体结合激活Wnt/PCP信号通路(属于非经典Wnt通路)。我们发现Wnt5b在非小细胞肺癌中高表达，并且与肺癌的淋巴结转移和不良预后密切相关；而先前我们证实Dvl-3主要通过非经典Wnt通路影响非小细胞肺癌细胞的侵袭。由此我们提出Wnt5b可能通过Fz活化Dvl-3，从而激活Wnt/PCP通路，进而促进非小细胞肺癌的恶性表型。我们拟双向调控非小细胞肺癌细胞的Wnt5b表达，转染Dvl-3结构域突变体(△PDZ/DEP-Dvl-3)，同时加入各种Fz亚型的抗体，通过Western blot、免疫共沉淀、成瘤实验等方法，在体内外证实Wnt5b通过Fz某亚型作用于Dvl-3某结构域(PDZ/DEP)从而活化Wnt/PCP通路，揭示Wnt5b激活Wnt/PCP通路促进非小细胞肺癌恶性表型的机制，为非小细胞肺癌的靶向治疗提供新的理论和实验依据。

Wnt5b, a ligand involved in the noncanonical Wnt pathway, which binds to the Fz receptor to activate Wnt/PCP pathway（noncanonical Wnt pathway）. We found that Wnt5b had high expression in non-small cell lung cancer（NSCLC）, which is closely associated with the lymph node metastasis and poor prognosis. Previously we reported that Dvl-3 affected NSCLC cell invasion mainly through noncanonical Wnt pathway. Based on the above, we propose that Wnt5b may activate Dvl-3 through Fz to promote Wnt/PCP pathway, and then promote the malignant phenotype of NSCLC. We intend to regulate Wnt5b expression by bidirectional control ways, transfect Dvl-3 expression plasmid with DEP or PDZ mutant to NSCLC cell，treat with the antibodies of different Fz subtypes, and then perform Western blot, co-immunoprecipitation, nude mouse xenograft model to confirm that Wnt5b works on PDZ/DEP domain of Dvl-3 through a subtype of Fz so as to activate Wnt/PCP signaling pathway, revealing the mechanism that Wnt5b activates Wnt/PCP pathway to promote the malignant phenotype of NSCLC, which could provide new theoretical and experimental evidence for the target treatment of NSCLC.