This study aims to investigate how Maspin affects the EMT and angiogenesis of gastric cancer (GC) cells via ITGB1/FAK pathway. Immunohistochemistry was used to evaluate the expressions of Maspin, ITGB1, FAK, E-cadherin, Vimentin, D2-40, and CD34 in GC and adjacent normal tissues from 160 patients. Then, the human GC cells with different degree of differentiation were transfected with Maspin CRISPR activation plasmid, ITGB1 siRNA and/or Maspin siRNA, followed by the following experiments, including qRT-PCR, western blotting, tube formation assay, Transwell assay and wound healing. GC tumor tissues manifested decreased Maspin with the activated ITGB1/FAK pathway. In tumor tissues, Maspin was negatively correlated with the expressions of ITGB1 and FAK, as well as Lauren’s classification, differentiation degree, and TNM stage. Besides, Maspin was negatively related with lymphatic vessel density (LVD) and microvessel density (MVD), Vimentin and VEGF, but was positive correlated with E-cadherin. Maspin expression decreased, but ITGB1 and p-FAK expressions increased gradually in MKN-28 (well differentiated), SGC-7901 (moderate differentiated), and MKN-45 (poorly differentiated). Maspin CRISPR and ITGB1 siRNA increased E-cadherin with the decreased Vimentin, VEGF and bFGF, and the reductions of tube length. In comparison with the ITGB1 siRNA group, cells in the Maspin siRNA + ITGB1 siRNA group presented the more evident EMT and angiogenesis. Furthermore, ITGB1 siRNA reduced the malignancies of GC cells, which could be restored by Maspin siRNA. Maspin was downregulated in GC tissues, which could inhibit the EMT and angiogenesis by blocking the ITGB1/FAK pathway, thereby decreasing cell invasion and migration of GC.

中文翻译：

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Maspin通过抑制ITB1 / FAK途径的EMT和血管生成来抑制胃癌中的细胞侵袭和迁移。

这项研究旨在调查Maspin如何通过ITGB1 / FAK途径影响EMT和胃癌（GC）细胞的血管生成。免疫组织化学用于评估Maspin，ITGB1，FAK，E-cadherin，Vimentin，D2-40和CD34在160例患者的GC和邻近正常组织中的表达。然后，用Maspin CRISPR激活质粒，ITGB1 siRNA和/或Maspin siRNA转染不同分化程度的人GC细胞，然后进行以下实验，包括qRT-PCR，western blotting，管形成测定，Transwell测定和伤口愈合。GC肿瘤组织通过激活的ITGB1 / FAK途径表现出Maspin减少。在肿瘤组织中，Maspin与ITGB1和FAK的表达以及Lauren的分类，分化程度和TNM分期呈负相关。除了，Maspin与淋巴管密度（LVD）和微血管密度（MVD），波形蛋白和VEGF呈负相关，但与E-钙粘蛋白呈正相关。Maspin表达下降，但ITGB1和p-FAK表达在MKN-28（高度分化），SGC-7901（中度分化）和MKN-45（低分化）中逐渐增加。Maspin CRISPR和ITGB1 siRNA增加E-钙黏着蛋白的波形蛋白，VEGF和bFGF降低，并且管长度减少。与ITGB1 siRNA组相比，Maspin siRNA + ITGB1 siRNA组中的细胞表现出更明显的EMT和血管生成。此外，ITGB1 siRNA减少了GC细胞的恶性肿瘤，可以通过Maspin siRNA进行恢复。Maspin在GC组织中表达下调，可通过阻断ITGB1 / FAK途径来抑制EMT和血管生成，从而减少GC的细胞侵袭和迁移。