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FAT10 is associated with the malignancy and drug resistance of non-small cell lung cancer

Authors Xue F, Zhu L, Meng Q, Wang L, Chen X, Zhao Y, Xing Y, Wang X, Cai L

Received 15 October 2015

Accepted for publication 31 March 2016

Published 19 July 2016 Volume 2016:9 Pages 4397—4409


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ram Prasad

Peer reviewer comments 3

Editor who approved publication: Professor Jianmin Xu

Feng Xue,1,2,* Lin Zhu,3,* Qing-wei Meng,1 Liyan Wang,2 Xue-song Chen,1 Yan-bin Zhao,1 Ying Xing,1 Xiao-yun Wang,1 Li Cai1

The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, 2Department of Medical Oncology, Heilongjiang Provincial Hospital, 3Department of Radiotherapy, Harbin Medical University Cancer Hospital, Harbin, People’s Republic of China

*These authors contributed equally to this work

Abstract: Lung cancer has become one of the leading causes of cancer mortality worldwide, and non-small-cell lung cancer (NSCLC) accounts for ~85% of all lung cancer cases. Currently, platinum-based chemotherapy drugs, including cisplatin and carboplatin, are the most effective treatment for NSCLC. However, the clinical efficacy of chemotherapy is markedly reduced later in the treatment because drug resistance develops during the treatment. Recently, a series of studies has suggested the involvement of FAT10 in the development and malignancy of multiple cancer types. In this study, we focused our research on the function of FAT10 in NSCLC, which has not been previously reported in the literature. We found that the expression levels of FAT10 were elevated in quick chemoresistance NSCLC tissues, and we demonstrated that FAT10 promotes NSCLC cell proliferation, migration, and invasion. Furthermore, the protein levels of FAT10 were elevated in cisplatin- and carboplatin-resistant NSCLC cells, and knockdown of FAT10 reduced the drug resistance of NSCLC cells. In addition, we gained evidence that FAT10 regulates NSCLC malignancy and drug resistance by modulating the activity of the nuclear factor kappa B signaling pathway.

Keywords: FAT10, NSCLC, malignancy, drug resistance, NFκB

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