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Metastasis-associated lung adenocarcinoma transcript 1 promotes the proliferation of chondro­sarcoma cell via activating Notch-1 signaling pathway

Authors Xu F, Zhang Z, Fang Y, Li X, Sun Y, Xiong C, Yan L, Wang Q

Received 6 November 2015

Accepted for publication 20 January 2016

Published 13 April 2016 Volume 2016:9 Pages 2143—2151

DOI https://doi.org/10.2147/OTT.S100003

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ram Prasad

Peer reviewer comments 3

Editor who approved publication: Dr Faris Farassati


Fengqin Xu,1,* Zhi-qiang Zhang,2,* Yong-chao Fang,2 Xiao-lei Li,2 Yu Sun,2 Chuan-zhi Xiong,2 Lian-qi Yan,2 Qiang Wang2

1Department of Orthopaedics, Hongquan Hospital, 2Department of Orthopaedics, Subei People’s Hospital, Yangzhou, Jiangsu Province, People’s Republic of China

*These authors contributed equally to this work

Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is identified to be overexpressed in several cancers. However, the role of MALAT-1 in chondrosarcoma is poorly understood.
Methods: The expression of MALAT-1 and Notch-1 signaling pathway was detected in chondrosarcoma tissues and chondrosarcoma cells by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to examine the cell viability of chondrosarcoma cells transfected with si-MALAT-1 or pcDNA-MALAT-1. Then the expression of Notch-1 signaling pathway was detected when MALAT-1 was upregulated or downregulated in chondrosarcoma cells. A subcutaneous chondrosarcoma cells xenograft model was used to confirm the effect of MALAT-1 on tumor growth in vivo.
Results: We found the increased expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma tissue and cells. MALAT-1 promoted the proliferation of chondrosarcoma cells. In addition, MALAT-1 activated the Notch-1 signaling pathway at posttranscriptional level in chondrosarcoma cells. Meanwhile, overexpression of Notch-1 reversed the effect of si-MALAT-1 on the proliferation of chondrosarcoma cells. Finally, we found that MALAT-1 promoted the tumor growth in a subcutaneous chondrosarcoma cells xenograft model, which confirmed the promoted effect of MALAT-1 on the tumor growth in vivo.
Conclusion: Taken together, our study demonstrated that MALAT-1 promoted the proliferation of chondrosarcoma cell via activating Notch-1 signaling pathway.

Keywords: MALAT-1, cell proliferation, chondrosarcoma, Notch-1, molecular pathophysiology

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