G-protein-coupled receptors (GPCRs) have been reported to participate in the occurrence and development of a variety of human cancers. CALCR is one of the hundreds of GPCRs, but its expression level and functional importance have never been investigated in non-small-cell lung cancer (NSCLC). In the present study, the protein expression level of CALCR was detected by immunohistochemical staining and western blot analysis. The Celigo cell counting assay was used to assess cell proliferation. Both the wound-healing assay and the transwell assay were performed to evaluate cell migration. Flow cytometric analysis was utilized to detect cell apoptosis and cell cycle. A mouse xenograft model was constructed to conduct the in vivo experiments. The results indicated that the CALCR expression was abundantly up-regulated in NSCLC and positively related to tumor infiltrate. Besides, CALCR knockdown could significantly suppress cell proliferation, migration, enhance apoptosis and arrest cell cycle. The in vivo study verified the inhibitory effects of CALCR knockdown on NSCLC tumorigenesis. The abovementioned results provided a reference for the treatment of NSCLC, that was, CALCR knockdown might be a considerable therapeutic strategy.

中文翻译：

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CALCR 敲低抑制非小细胞肺癌的发生和进展。

据报道，G蛋白偶联受体（GPCRs）参与多种人类癌症的发生和发展。CALCR 是数百个 GPCR 之一，但其表达水平和功能重要性从未在非小细胞肺癌 (NSCLC) 中得到研究。本研究通过免疫组化染色和蛋白质印迹分析检测CALCR的蛋白表达水平。Celigo细胞计数测定用于评估细胞增殖。进行伤口愈合试验和 transwell 试验以评估细胞迁移。流式细胞术分析用于检测细胞凋亡和细胞周期。构建小鼠异种移植模型以进行体内实验。结果表明CALCR表达在NSCLC中大量上调并且与肿瘤浸润呈正相关。此外，CALCR敲低可以显着抑制细胞增殖、迁移、增强细胞凋亡和阻滞细胞周期。体内研究证实了 CALCR 敲低对 NSCLC 肿瘤发生的抑制作用。上述结果为NSCLC的治疗提供了参考，即CALCR敲低可能是一个相当重要的治疗策略。