Research Papers:
SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
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Abstract
Jun Sheng1,*, Mengchen Yin2,*, Zhengwang Sun3,*, Xia Kang1, Da Liu1, Kai Jiang1, Jia Xu4,**, Feixing Zhao5,**, Qunfeng Guo3,** and Wei Zheng1,**
1Department of Orthopedics, Chengdu Military General Hospital, Chengdu, Sichuan, China
2Department of Orthopedics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
3Department of Orthopedics, Changzheng Hospital, The Second Military Medical University, Shanghai, China
4Department of Personnel Office, Traditional Chinese Medical Hospital of Zhuji, Zhuji, Zhejiang, China
5Department of Pathology, Zhuji People’s Hospital of Zhejiang Province, Zhuji, Zhejiang, China
*These authors have contributed equally to this work
**Authors for correspondence with equal contribution
Correspondence to:
Wei Zheng, email: [email protected]
Jia Xu, email: [email protected]
Feixing Zhao, email: [email protected]
Qunfeng Guo, email: [email protected]
Zhengwang Sun, email: [email protected]
Keywords: SPC24; osteosarcoma; Ras/Raf/MEK/ERK signal pathway; E-cadherin
Received: April 19, 2017 Accepted: August 29, 2017 Published: October 27, 2017
ABSTRACT
In this study, we investigated the role of the spindle checkpoint protein SPC24 in osteosarcoma progression. SPC24 knockdown in 143B and U2OS osteosarcoma cells decreased cell growth, survival and invasiveness. The SPC24 knockdown cells also exhibited low EGFR, Ras and phospho-ERK levels and high E-cadherin levels, suggesting inhibition of EGFR/Ras/ERK signaling and epithelial-to-mesenchymal transitioning. Xenografted SPC24 knockdown osteosarcoma cells showed reduced tumor growth in nude mice with decreased EGFR and phospho-ERK levels and increased E-cadherin levels. By contrast, human osteosarcoma tissue samples showed high SPC24 and phospho-ERK levels and low E-cadherin levels. These results suggest SPC24 promotes osteosarcoma progression by increasing EGFR/Ras/ERK signaling.
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