胃癌已成为全球癌症相关死亡的第四大主要原因。本研究旨在探讨RGS1在胃癌体外和体内的作用。我们确定了NCIN87细胞及耐药性NCIN87细胞（NCIN87-DR）的增殖、迁移、侵袭和集落形成。细胞凋亡和细胞周期通过流式细胞术进行检测。建立了RGS1基因沉默载体（pLVshshRGS1）和异种移植瘤小鼠模型。使用西方印迹法检测了RGS1和上皮间质转化（EMT）相关标志物，包括E-cadherin（E-cad）、N-cadherin（N-cad）、Slug和Vimentin。测量了异种移植瘤小鼠的肿瘤大小，并使用免疫组化法检测Ki67表达。与NCIN87细胞相比，NCIN87-DR细胞的增殖、迁移和侵袭明显降低（p <0.05）。NCIN87-DR细胞显示明显的早期凋亡，并且细胞周期发生明显改变。与NCIN87细胞相比，NCIN87-DR细胞表现出明显较高的RGS1表达（p <0.01）。与NCIN87细胞相比，NCIN87-DR细胞的E-cad表达显著降低（p <0.01），而N-cad（p <0.05）、Slug（p <0.01）和Vimentin（p <0.05）的表达显著增加。与未处理的NCIN87-DR细胞相比，RGS1基因沉默显著降低了NCIN87-DR细胞的增殖（p <0.01）。与未经RGS1沉默处理的细胞相比，RGS1基因沉默处理的NCIN87-DR细胞的免疫接种明显抑制了异种移植瘤小鼠的肿瘤生长（p <0.05）。与未经RGS1沉默处理的细胞相比，RGS1基因沉默处理的NCIN87-DR细胞免疫接种显著降低了肿瘤组织中的Ki67表达。总之，RGS1基因沉默可以减少NCIN87-DR细胞的增殖并抑制体内肿瘤生长。因此，RGS1可作为胃癌治疗的抗肿瘤靶点。© TÜBİTAK.

Gastric cancer is becoming the 4th leading cause of cancer-associated death worldwide. The purpose of this study was to investigate the role of RGS1 in gastric cancer in vitro and in vivo. Proliferation, migration, invasion, and colony formation of NCIN87 cells and drug-resistant NCIN87 cells (NCIN87-DR) were determined. Cell apoptosis and cell cycle were examined using a flow cytometry assay. RGS1 gene knock-down vector (pLVshshRGS1) and Xenograft tumor mouse model was generated. RGS1 and epithelial-mesenchymal transition (EMT) associated markers, including E-cadherin (E-cad), N-cadherin (N-cad), Slug, and Vimentin were detected using a western blotting assay. Tumor size of Xenograft tumor mouse was measured and Ki67 expression was detected using the immunohistochemical assay. NCIN87-DR cells demonstrated significantly lower proliferation, migration, and invasion compared to those of NCIN87 cells (p < 0.05). NCIN87-DR cells showed obvious early apoptosis and displayed obvious alterations for the cell cycle. NCIN87-DR cells exhibited predominantly higher RGS1 expression than that in NCIN87 cells (p < 0.01). E-cad expression was markedly decreased (p < 0.01) and N-cad (p < 0.05), Slug (p < 0.01), Vimentin (p < 0.05) expressions were significantly increased in NCIN87-DR cells than those in NCIN87 cells. RGS1 gene silence remarkably reduced NCIN87-DR proliferation compared to that in NCIN87-DR cells without treatment (p < 0.01). RGS1 gene-silenced NCIN87-DR cell immunization predominantly inhibited tumor growth in Xenograft tumor mouse than that without RGS1 silence (p < 0.05). RGS1 gene-silenced NCIN87-DR cell immunization significantly downregulated Ki67 expression in tumor tissues compared with that without RGS1 silence. In conclusion, RGS1 gene silence reduced the proliferation of NCIN87-DR cells in vitro and inhibited tumor growth in vivo. Therefore, RGS1 served as an antitumor target for the gastric cancer treatment.© TÜBİTAK.