在这项研究中,我们研究了PIK3R6的作用,PIK3R6是PI3Kγ的调节亚基,以其促进肿瘤的特性而闻名,肾透明细胞癌(CCRCC)。利用UALCAN网站,我们发现PIK3R6在CCRCC中上调,与较低的生存率有关。我们使用免疫组织化学比较了CCRCC肿瘤组织和邻近正常组织中的PIK3R6表达。在786-O和ACHN细胞系中,RNA干扰诱导的PIK3R6敲低,我们进行了CCK-8,集落形成,Edu染色,流式细胞术,伤口愈合,和transwell分析。结果显示PIK3R6沉默降低细胞增殖,迁移,和入侵,诱导G0/G1期阻滞和凋亡。分子分析显示CDK4、CyclinD1、N-cadherin、Vimentin,Bcl-2、p-PI3K和p-AKT,随着caspase-3,Bax,CCRCC细胞中的E-cadherin水平。此外,抑制PIK3R6阻碍肿瘤生长。这些发现表明PIK3R6在CCRCC细胞增殖和转移中的重要作用。将其作为潜在的治疗靶点。
In this research, we investigated the role of PIK3R6, a regulatory subunit of PI3Kγ, known for its tumor-promoting properties, in clear cell renal cell carcinoma (CCRCC). Utilizing the UALCAN website, we found PIK3R6 upregulated in CCRCC, correlating with lower survival rates. We compared PIK3R6 expression in CCRCC tumor tissues and adjacent normal tissues using immunohistochemistry. Post RNA interference-induced knockdown of PIK3R6 in 786-O and ACHN cell lines, we performed CCK-8, colony formation, Edu staining, flow cytometry, wound healing, and transwell assays. Results showed that PIK3R6 silencing reduced cell proliferation, migration, and invasion, and induced G0/G1 phase arrest and apoptosis. Molecular analysis revealed decreased CDK4, Cyclin D1, N-cadherin, Vimentin, Bcl-2, p-PI3K and p-AKT, with increased cleaved caspase-3, Bax, and E-cadherin levels in CCRCC cells. Moreover, inhibiting PIK3R6 hindered tumor growth. These findings suggest a significant role for PIK3R6 in CCRCC cell proliferation and metastasis, presenting it as a potential therapeutic target.