Purpose: Lung cancer has been recognized as the most fatal malignant tumor with the highest morbidity and mortality in recent years.
Materials and Methods: 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.
Results: In vitro loss-of-function study utilizing LMNB1 knockdown LUAD cell lines demonstrated that depletion of LMNB1  inhibited development of LUAD through regulating cell proliferation, cell apoptosis, cell cycle and cell motility. Decreased tumorigenesis of LMNB1  knockdown LUAD cells was proved in mice xenograft models. Moreover, the mechanism by which LMNB1  promotes LUAD was explored through the expression evaluation of apoptosis-related proteins and cancer-related signaling pathways.
Conclusion: In conclusion, our study identified LMNB1  as a tumor promotor and a potential therapeutic target in LUAD.
Keywords: lung cancer, lung adenocarcinoma, LMNB1 , cell proliferation, cell apoptosis