Introduction/Objective: This study aimed to explore the expression of cyclin-dependent kinase subunit 2 (CKS2) in tissues and cells in non-small-cell lung cancer (NSCLC) and the function mechanism of CKS2 in NSCLC cell growth and tumorigensis. Methods: After transfecting NCI-H2170 cells with short-hair RNA (shRNA), an shCKS2 gene-silencing model was established. The cells were divided into a shRNA group and shNC group. For overexpression cell lines, we used the same method to establish the NCI-H2170-CKS2 cell lines. Cell Count Kit-8 assay and colony formation assay were used to determine cell viability and cell growth, respectively. Propidium iodide staining was used to determine cell cycle progression. The mRNA expression of CKS2 and protein expression of CKS2, p21, p53, and PTEN were determined by RT-qPCR and Western blotting, respectively. The expression of CKS2, p53, and Ki67 in tissues was determined by immunohistochemical stain. The in vivo tumorigenesis assays were used to determine the ability of CKS2 in tumor growth. Results: The results of RT-qPCR and Western blotting assay revealed that CKS2 upregulated expression in NSCLC tissues and cells. The results of the CCK-8 assay revealed that the shRNA group exhibited significantly lower cell viability and foci formation than the empty plasmid group, while CKS2 overexpression induces cell growth and cell cycle progression. The result of nude mice suggested that CKS2 knockdown expression suppressed tumorigenesis in the in vivo animal model. Conclusions: Our study suggests that CKS2 could be a biomarker in the progression and prognosis of NSCLC.
Pathobiology

中文翻译：

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CKS2 通过下调细胞周期蛋白依赖性激酶抑制剂促进非小细胞肺癌的生长

简介/目的：本研究旨在探讨细胞周期蛋白依赖性激酶亚基2（CKS2）在非小细胞肺癌（NSCLC）组织和细胞中的表达以及CKS2在NSCLC细胞生长和肿瘤发生中的作用机制。方法：用短毛RNA（shRNA）转染NCI-H2170细胞后，建立了shCKS2基因沉默模型。将细胞分为shRNA组和shNC组。对于过表达细胞系，我们使用相同的方法建立NCI-H2170-CKS2细胞系。Cell Count Kit-8 测定和集落形成测定分别用于确定细胞活力和细胞生长。碘化丙啶染色用于确定细胞周期进程。分别通过 RT-qPCR 和蛋白质印迹法测定 CKS2 的 mRNA 表达和 CKS2、p21、p53 和 PTEN 的蛋白表达。通过免疫组织化学染色测定组织中CKS2、p53和Ki67的表达。体内肿瘤发生测定用于确定CKS2在肿瘤生长中的能力。结果：RT-qPCR和Western印迹分析结果显示CKS2在NSCLC组织和细胞中上调表达。CCK-8 测定结果显示，shRNA 组的细胞活力和病灶形成明显低于空质粒组，而 CKS2 过表达诱导细胞生长和细胞周期进程。裸鼠的结果表明，CKS2 敲低表达抑制了体内动物模型中的肿瘤发生。结论：我们的研究表明，CKS2 可能是 NSCLC 进展和预后的生物标志物。
病理学