Zhang Jin, Ma Qianli, Han Yu, Wen Huanshun, Zhang Zhenrong, Hao Yang, Xiao Fei, Liang Chaoyang
Department of Thoracic Surgery, China-Japan Friendship Hospital, Beijing, China.
J Thorac Dis. 2022 Feb;14(2):507-514. doi: 10.21037/jtd-22-116.
Lung cancer is still one of the most common causes of cancer-related mortality, and the overall survival is less than 5%. It is important and necessary to elucidate the mechanism of lung cancer progression. Recently, more and more research has demonstrated that many ribosomal proteins (RPs) are dysregulated in tumors. Among these RPs, ribosomal protein L6 (RPL6) is reported to promote cell growth and cell cycle progression in gastric cancer cells through upregulating cyclin E. However, its function in lung cancer is still unknown.
We first explored RPL6 expression in lung cancer samples. Next, we used gene knockdown to analyze the unknown regulatory role of RPL6 in lung cancer carcinoma and lung cancer cell lines. Furthermore, we explored the potential signaling pathway of RPL6 with Western blotting.
In this study, we demonstrated that RPL6 expression was highly expressed in lung cancer tissues and lung cancer cell lines. RPL6 downregulation inhibited H1299 and H2975 cell proliferation, migration and induced cell apoptosis. Also RPL6 downregulation increased the protein levels of cleaved caspase-3 and Bax, while decreasing the protein level of B-cell lymphoma 2 (Bcl-2). Western blotting results showed that proteins activating the AKT signaling pathway, such as p-AKT and p-S6, were downregulated in RPL6 knockdown lung cancer cells.
These findings show that RPL6 can be used as a potential therapeutic and preventive biomarker in lung cancer treatment and prognosis by regulating the AKT signaling pathway.
肺癌仍然是癌症相关死亡的最常见原因之一，总体生存率低于5%。阐明肺癌进展机制具有重要意义且很有必要。最近，越来越多的研究表明许多核糖体蛋白（RPs）在肿瘤中表达失调。在这些核糖体蛋白中，据报道核糖体蛋白L6（RPL6）通过上调细胞周期蛋白E促进胃癌细胞的生长和细胞周期进程。然而，其在肺癌中的功能仍然未知。
我们首先探究了RPL6在肺癌样本中的表达。接下来，我们使用基因敲低来分析RPL6在肺癌组织和肺癌细胞系中的未知调控作用。此外，我们通过蛋白质印迹法探究了RPL6的潜在信号通路。
在本研究中，我们证明RPL6在肺癌组织和肺癌细胞系中高表达。RPL6下调抑制了H1299和H2975细胞的增殖、迁移并诱导细胞凋亡。RPL6下调还增加了裂解的半胱天冬酶-3和Bax的蛋白水平，同时降低了B细胞淋巴瘤2（Bcl-2）的蛋白水平。蛋白质印迹结果显示，在RPL6敲低的肺癌细胞中，激活AKT信号通路的蛋白，如p-AKT和p-S6，表达下调。
这些发现表明，RPL6可通过调节AKT信号通路，作为肺癌治疗和预后的潜在治疗和预防生物标志物。
