AIM: To investigate the expression of actin filament-associated protein 1-like 2 (AFAP-1L2) in different pancreatic cancer cell lines, the effect of AFAP-1L2 on cell proliferation, cell cycle and apoptosis, and the possible mechanism. METHODS: Western blot and real-t ime quantitative PCR (qRT-PCR) were used to detect the AFAP-1L2 protein and mRNA expression in PANC-1, MiaPaCa-2, Colo-357, BXPC-3, SW1990 and CFPAC-1 cell lines (having different differentiation degrees). siAFAP-1L2 plasmid was constructed and transfected into MiaPaCa-2 cell to downregulate the expression of AFAP1L2. Proteins of the phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) pathway were detected by Western blot and qRT-PCR after siAFAP-1L2 transfection. Proliferation was detected by MTT assay. Cell cycle and apoptosis were detected by flow cytometry. RESULTS: Western blot and qRT-PCR analyses showed that AFAP-1L2 was correlated with differentiation degree, and the expression was higher in cell lines with low differentiation than in those with moderate or high differentiation. PI3KCA protein expression in the siAFAP-1L2 group was lower than that in the MOCK and siRNA control groups (F = 20.16, P = 0.0022). α-Akt mRNA expression in the siAFAP-1L2 group was higher than that in the MOCK and siRNA control groups (F = 7.719, P = 0.0219); α-pAkt protein expression in the siAFAP1L2 group was lower than that in MOCK and siRNA control groups (F = 5.507, P = 0.0439). PI3KCA mRNA expression in the siAFAP-1L2 group was lower than that in the AFAP-1L2 and siRNA control groups (F = 20.16, P = 0.0022). α-Akt mRNA expression in the siAFAP-1L2 group was higher than that in the MOCK and siRNA control groups (F = 6.068, P = 0.0362); α-pAkt mRNA expression in the siAFAP-1L2 group was lower than that in the MOCK and siRNA control groups (F = 10.33, P = 0.0114). AFAP-1L2通过PI3K/Akt通路影响胰腺癌细胞增殖及凋亡 刘 博, 戚 诚, 刘学臣, 赵晓东 在线投稿: http://www.baishideng.com/wcjd/ch/index.aspx 帮助平台: http://www.wjgnet.com/esps/helpdesk.aspx DOI: 10.11569/wcjd.v23.i28.4490 世界华人消化杂志 2015年10月8日; 23(28): 4490-4498 ISSN 1009-3079 (print) ISSN 2219-2859 (online) © 2015年版权归百世登出版集团有限公司所有. 基础研究 BASIC RESEARCH ® ■同行评议者 刘 亮 , 副 主 任 医 师, 复旦大学胰腺 癌研究所; 复旦大 学附属肿瘤医院 胰腺肝胆外科 刘博, 等. AFAP-1L2通过PI3K/Akt通路影响胰腺癌细胞增殖及凋亡 2015-10-08|Volume 23|Issue 28| WCJD|www.wjgnet.com 4491 ■研发前沿 对胰腺癌预后评 估的靶基因的检 测及治疗靶点的 探索是胰腺癌靶 向治疗的研究热 点 , 深入探讨靶 基因对胰腺癌细 胞的调控机制是 目前研究的重点, 对治疗靶点的筛 查手段及应用于 临床的有效性和 意义是亟待解决 的问题. MTT assay showed that the proliferation of MiaPaCa-2 cells at 48 h, 72 h, and 96 h was inhibited after siAFAP-1L2 transfection (F = 3.924, P < 0.05; F = 6.812, P < 0.01; F = 7.003, P < 0.01). Flow cytometry showed that cells in G1 phase were increased, but those in G2 and S phases were decreased (F = 4.87, 5.26, 4.94, P < 0.05 for all). The apoptosis rate of MiaPaCa-2 cell was increased after siAFAP-1L2 transfection (F = 7.231, P < 0.01). CONCLUSION: AFAP-1L2 expression is associated with cell differentiation. AFAP-1L2 modulates cell proliferation, cell cycle and apoptosis via the PI3K/Akt pathway. AFAP-1L2 is a target candidate for pancreatic cancer therapy. © 2015 Baishideng Publishing Group Inc. All rights reserved.