Tang Dan, Luo Haihai, Xie An, He Zhichun, Zou Bin, Xu Fei, Zhang Wei, Xu Xinping
Jiangxi Institute of Respiratory Disease, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China.
Department of General Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China.
Cancer Manag Res. 2021 Mar 18;13:2633-2642. doi: 10.2147/CMAR.S275874. eCollection 2021.
Lung cancer has been recognized as the most fatal malignant tumor with the highest morbidity and mortality in recent years.
In this study, we found that LMNB1, which is an important component protein of the nuclear skeleton, was significantly upregulated in lung adenocarcinoma (LUAD) and correlated with the pathological stage as well as lymphatic metastasis.
In vitro loss-of-function study utilizing knockdown LUAD cell lines demonstrated that depletion of inhibited development of LUAD through regulating cell proliferation, cell apoptosis, cell cycle and cell motility. Decreased tumorigenesis of knockdown LUAD cells was proved in mice xenograft models. Moreover, the mechanism by which promotes LUAD was explored through the expression evaluation of apoptosis-related proteins and cancer-related signaling pathways.
In conclusion, our study identified as a tumor promotor and a potential therapeutic target in LUAD.
肺癌已被公认为近年来发病率和死亡率最高的最致命恶性肿瘤。
在本研究中，我们发现核骨架的重要组成蛋白LMNB1在肺腺癌（LUAD）中显著上调，且与病理分期以及淋巴转移相关。
利用敲低LUAD细胞系进行的体外功能丧失研究表明，敲低抑制了LUAD的发展，其机制是通过调节细胞增殖、细胞凋亡、细胞周期和细胞运动。在小鼠异种移植模型中证实了敲低LUAD细胞的肿瘤发生减少。此外，通过对凋亡相关蛋白和癌症相关信号通路的表达评估，探索了促进LUAD的机制。
总之，我们的研究确定为LUAD中的肿瘤促进因子和潜在治疗靶点。
