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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Inhibition of Cell-surface Molecular GPR87 With GPR87-suppressing Adenoviral Vector Disturb Tumor Proliferation in Lung Cancer Cells
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Inhibition of Cell-surface Molecular GPR87 With GPR87-suppressing Adenoviral Vector Disturb Tumor Proliferation in Lung Cancer Cells

机译：抑制细胞表面分子GPR87与GPR87抑制腺病毒载体干扰肺癌细胞中肿瘤增殖的抑制作用

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Background/Aim: GPR87 is a member of the cell surface molecular G protein-coupled receptors (GPCR) family and suggested to contribute to the viability of human tumor cells. Its tumor-specific expression and cell surface location make it a potential molecule for targeted therapy. In the present study, we aimed to examine the effect of silencing GPR87 expression and explore the possibility of establishing gene therapy against GPR87-overexpressing lung cancer. Materials and Methods: Twenty malignant cell lines were investigated and GPR87-overexpressing H358 and PC9 lung cancer cells were subjected to inhibiting experiments. A short hairpin siRNA targeting the GPR87 gene was transformed into an adenoviral vector (Ad-shGPR87). Real-time RT-PCR and western blot analyses were performed to evaluate gene and protein expression. Tumors derived from human H358 cells were subcutaneously implanted in nude mice for in vivo experiments. Results and Conclusion: About 50% (10/20) malignant cells showed GPR87-overexpression, especially for lung cancer cells (70%, 7/10). Ad-shGPR87 effectively down-regulated the GPR87 expression, and significantly inhibited the cell proliferation in GPR87-overexpressing H358 and PC9 cells. Treatment with Ad-shGPR87 exerted a significant antitumor effect against the GPR87-expressing H358 xenografts. In addition, the gene expression of H3.3, a recently proved activator for GPR87 transcription, was positively correlated with GPR87 gene expression. Furthermore, a significant decrease of KRAS and c-Myc expression was observed in both cell lines after Ad-shGPR87 infection. In conclusion, GPR87 may play a critical role in cancer cell proliferation, and indicate its potential as a novel target for lung cancer treatment.
机译：背景/目的：GPR87是细胞表面分子G蛋白偶联受体（GPCR）家族的成员，并建议有助于人肿瘤细胞的活力。其肿瘤特异性表达和细胞表面位置使其成为靶向治疗的潜在分子。在本研究中，我们旨在研究沉默GPR87表达的效果，探讨与GPR87过表达肺癌建立基因治疗的可能性。材料和方法：研究了20个恶性细胞系，对H358和PC9肺癌细胞进行了GPR87-过表达H358和PC9肺癌细胞抑制实验。将靶向GPR87基因的短发夹siRNA转化为腺病毒载体（Ad-SHGPR87）。进行实时RT-PCR和Western印迹分析以评估基因和蛋白质表达。将衍生自人H358细胞的肿瘤皮下植入体内实验中的裸鼠中。结果和结论：约50％（10/20）恶性细胞显示GPR87过表达，特别是对于肺癌细胞（70％，7/10）。 AD-SHGPR87有效地下调了GPR87表达，并显着抑制了GPR87-过表达H358和PC9细胞中的细胞增殖。用AD-SHGPR87治疗施加对表达GPR87的H358异种移植物的显着抗肿瘤效应。此外，H3.3的基因表达是最近被证明的用于GPR87转录的活化剂，与GPR87基因表达呈正相关。此外，在AD-SHGPR87感染后，在两种细胞系中观察到KRAS和C-MYC表达的显着降低。总之，GPR87可能在癌细胞增殖中发挥关键作用，并表明其作为肺癌治疗的新靶标的潜力。

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