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AMPH-1 As A Critical Tumor Suppressor That Inhibits Osteosarcoma Progression

Authors Zhang H, Liu Y, Xu K, Mao K, Han W, Xu F, Wan W, Sun Y

Received 24 June 2019

Accepted for publication 22 October 2019

Published 25 November 2019 Volume 2019:11 Pages 9913—9919


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Ahmet Emre Eskazan

Haiyun Zhang,1,* Yujie Liu,2,* Kehan Xu,2,* Kai Mao,1 Weidong Han,1 Feifan Xu,1 Wei Wan,2 Yajun Sun3

1Department of Laboratory Medicine, The Sixth People’s Hospital of Nantong, Jiangsu 226000, People’s Republic of China; 2Department of Orthopedic Oncology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, People’s Republic of China; 3Department of Laboratory Medicine, The Fourth People’s Hospital of Nantong, Jiangsu 226000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yajun Sun; Wei Wan
Department of Laboratory Medicine, The Fourth People’s Hospital of Nantong, Chenggang Road, Jiangsu 226000, People’s Republic of China

Introduction: Amphiphysin 1 (AMPH-1) is involved in endocytosis, and its expression is upregulated in osteosarcoma compared with osteofibrous dysplasia.
Methods: We investigated the role of AMPH-1 in osteosarcoma cells via both gain-of-function and loss-of-function experiments.
Results: Knockdown of AMPH-1 in osteosarcoma cells promoted cell cycle progression and cell proliferation and attenuated apoptosis. Notably, silencing AMPH-1 increased osteosarcoma progression in a mouse tumor model. The results obtained upon AMPH-1 knockdown and AMPH-1 overexpression indicates that AMPH-1 is involved in regulating MEK/ERK signaling.
Conclusion: These data suggest that AMPH-1 plays an important role in osteosarcoma and may represent a novel therapeutic target for osteosarcoma treatment.

Keywords: AMPH-1, osteosarcoma, ERK signaling pathway

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