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Silencing LMNB1 Contributes to the Suppression of Lung Adenocarcinoma Development

Authors Tang D, Luo H, Xie A, He Z, Zou B, Xu F, Zhang W, Xu X

Received 11 August 2020

Accepted for publication 27 February 2021

Published 18 March 2021 Volume 2021:13 Pages 2633—2642

DOI https://doi.org/10.2147/CMAR.S275874

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly


Dan Tang,1,2,* Haihai Luo,1,* An Xie,3 Zhichun He,1 Bin Zou,4 Fei Xu,1 Wei Zhang,1 Xinping Xu1

1Jiangxi Institute of Respiratory Disease, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China; 2Department of General Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China; 3Jiangxi Institute of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China; 4Department of Thoracic Surgery, Jiangxi Cancer Hospital, Nanchang, Jiangxi, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xinping Xu; Wei Zhang
Jiangxi Institute of Respiratory Disease, The First Affiliated Hospital of Nanchang University, No. 17 Yongwai St, Nanchang, Jiangxi, 330006, People’s Republic of China
Email [email protected]; [email protected]

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

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