恶性黑色素瘤的发病率和病死率在逐年增长，引发广泛关注。目前恶性黑色素瘤的治疗方式主要为手术、化疗和靶 向治疗，总体疗效极差。然而，PD-1抗体治疗恶性黑色素瘤的成功，使广大研究者把希望聚焦于生物免疫治疗。肿瘤浸润淋巴细 胞（tumor infiltrating lymphocyte，TIL）是从肿瘤组织分离出的淋巴细胞，经体外扩增后得到的能够杀伤肿瘤细胞的细胞群，具有 高杀瘤活性和高靶向性特点。临床试验研究发现，TIL对恶性黑色素瘤治疗效果显著且稳定，但其临床疗效尚未完全阐明。本文 对TIL免疫治疗的发展及其在恶性黑色素瘤治疗中的研究新进展作一综述，以期为恶性黑色素瘤的治疗提供新的策略。

Objective: To observe the effect of SHIP1 on NSCLC cell proliferation. Methods: The CDS region of human SHIP1 gene was obtained by inquiring NCBI Gene database and was inserted into the vector pTSB-CMV-MCS-SBP-3Flag-EGFP to construct SHIP1 over-expression plasmid, which was further used to construct SHIP1 overexpression lentivirus. SHIP1 over-expressed lentiviruses were used to transfect A549, SPCA-1 and PC-9 cell lines to construct SHIP1 overexpressed NSCLC cell line. Western blotting and qRT-PCR were used to determine the protein and mRNAexpression of SHIP1. The MTT assay and Clone formation assay were used to examine the cell proliferation ability and clone formation ability of PC-9 cells overexpressed SHIP1; Western blotting was performed to examine the level of AP-1 proteins. Results: The sequencing result suggested that the SHIP1 eukaryotic over-expression plasmid was successfully constructed. A519, SPCA-1 and PC-9 cells with SHIP1 over-expression were observed to display uniform green fluorescence under fluorescent microscopy. Compared with negative control group, the mRNA and protein levels of SHIP1 were significantly increased in SHIP1 overexpressed cells (all P<0.01). The over-expression of SHIP1 suppressed the abilities of proliferation and clone formation in PC-9 cells (all P<0.01), and down-regulated the expression of p-c-Jun and FosB etc. Conclusion: The SHIP1 overexpressed NSCLC cell lines were successfully established, and the over-expression of SHIP1 suppressed the cell proliferation ability by inhibitingAP-1 proteins in NSCLC cell lines.