免疫逃避是肿瘤细胞通过逃避免疫细胞的识别和攻击而加速生长和转移的过程。SNF5是SWI/SNF的核心亚基之一,参与多种恶性肿瘤的发展。然而,SNF5在非小细胞肺癌(NSCLC)中的作用以及SNF5调节免疫逃避的机制尚不清楚。基于此,我们通过癌症基因组图谱(TCGA)数据库分析了SNF5的表达和肺癌组织的总生存期.然后,我们使用慢病毒感染和siRNA在NSCLCA549和NCI-H1299细胞中进行了SNF5的基因获得和功能丧失实验,分别。我们研究了这些细胞的增殖和免疫逃避。我们进一步摸索了SNF5对NSCLC细胞免疫逃避的机制。我们的数据显示SNF5在肺癌组织中明显高于正常肺组织。此外,SNF5促进NSCLC细胞增殖和免疫逃避相关基因的表达。同时,当与T细胞共培养时,过表达的SNF5降低了A549细胞的死亡率。此外,SNF5通过激活NSCLC细胞中的信号转导和转录激活因子(STAT3)/磷酸化-STAT3通路来调节免疫逃避。一起,我们的研究结果验证了SNF5作为肿瘤癌基因,为NSCLC治疗提供了新的靶点.
Immune evasion is the process that tumor cells accelerate growth and metastasis by evading the recognition and attack of immune cells. SNF5 is one of the core subunits of SWI/SNF, which is involved in the development of a variety of malignancies. However, the functions of
SNF5 in Non-Small Cell Lung Cancer (NSCLC) and the mechanism of
SNF5 regulates immune evasion are still unclear. Based on this, we analyzed the expression of
SNF5 and overall survival of lung cancer tissues through the cancer genome atlas (TCGA) database. Then we performed genetic gain and loss of function experiments with
SNF5 using lentivirus infection and siRNA in NSCLC A549 and NCI-H1299 cells, respectively. We investigated the proliferation and immune evasion of these cells. We further explored the mechanism of
SNF5 on NSCLC cells immune evasion. Our data showed that SNF5 was significantly increased in lung cancer tissues than that in normal lung tissues. Furthermore, SNF5 promoted NSCLC cells proliferation and the expressions of immune evasion-related genes. Meantime, overexpressed
SNF5 reduced mortality of A549 cells when co-cultured with T cells. Moreover, SNF5 regulated the immune evasion by activating the signal transducer and activator of transcription (STAT3)/ phospho-STAT3 pathway in NSCLC cells. Together, our results validate SNF5 as a tumor oncogene and provide a new target for NSCLC treatment.