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目的:检测WNT5A在小细胞肺癌(small cell lung cancer,SCLC)中的表达及其促细胞迁移作用的机制。方法:采用免疫组化的方法检测79例SCLC和25例正常肺组织中WNT5A的表达量。通过细胞划痕和Transwell小室检测WNT5A及JNK对SCLC细胞系DMS153迁移能力的作用,应用Western blot检测干扰WNT5A后磷酸化JNK含量的变化。结果:WNT5A在SCLC中表达高于正常肺组织,并且与肿瘤的临床分期、淋巴转移及远处转移相关,WNT5A的表达与神经元特性烯醇化酶(NSE)、胃泌素释放肽前体(Pro-GRP)也有明显相关性。干扰WNT5A导致DMS153迁移能力下降,应用JNK抑制剂SP600125能够阻止WNT5A造成的细胞迁移增加。结论:WNT5A在SCLC中高表达,并且与肿瘤的转移相关,WNT5A通过磷酸化JNK促进SCLC细胞迁移,并且可以作为SCLC的预测指标和治疗靶点。
Objective: To investigate the mechanism of WNT5A expression in small cell lung cancer (SCLC) and its role in cell migration. Methods: The expression of WNT5A in 79 cases of SCLC and 25 cases of normal lung tissue was detected by immunohistochemistry. The effect of WNT5A and JNK on the migration ability of SCLC cell line DMS153 was detected by cell scratch and Transwell chambers. The changes of phosphorylated JNK content after WNT5A interference were detected by Western blot. Results: The expression of WNT5A in SCLC was higher than that in normal lung tissue, and was correlated with the clinical stage, lymphatic metastasis and distant metastasis. The expression of WNT5A was correlated with neuron specific enolase (NSE), gastrin-releasing peptide precursor Pro-GRP) is also significantly related. Disruption of WNT5A led to decreased migration of DMS153, and the use of JNK inhibitor SP600125 prevented an increase in cell migration caused by WNT5A. CONCLUSIONS: WNT5A is highly expressed in SCLC and is associated with tumor metastasis. WNT5A promotes SCLC cell migration through phosphorylation of JNK and may serve as a predictive and therapeutic target for SCLC.