J Cancer 2017; 8(8):1362-1370. doi:10.7150/jca.18031

Research Paper

Osteopontin is Critical for Hyperactive mTOR-Induced Tumorigenesis in Oral Squamous Cell Carcinoma

Ning Gan1, 2, 3, 4, Sihai Zou1, 2, 3, Wenming Hang1, 2, 3, Deqin Yang1, 2, 3, Xuemei Zhang4, Yibing Yin4✉

1. Stomatological Hospital of Chongqing Medical University, Chongqing 401147, China;
2. Chongqing key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing 401147, China;
3. Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing 401147, China;
4. Department of Laboratory Medicine, Key Laboratory of Diagnostic Medicine (Ministry of Education), Chongqing Medical University, Chongqing 400016, China.

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Gan N, Zou S, Hang W, Yang D, Zhang X, Yin Y. Osteopontin is Critical for Hyperactive mTOR-Induced Tumorigenesis in Oral Squamous Cell Carcinoma. J Cancer 2017; 8(8):1362-1370. doi:10.7150/jca.18031. Available from https://www.jcancer.org/v08p1362.htm

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Mechanistic target of rapamycin (mTOR) plays a critical role in the development of oral squamous cell carcinoma (OSCC), but the underlying mechanisms remain poorly understood. Here we have demonstrated that the expression of osteopontin (OPN) was dramatically up-regulated in OSCC tissues and cell lines. Moreover, reduction of OPN suppressed cell proliferation, colony formation, and in vivo tumorigenic ability of OSCC cell lines Tca8113. In addition, there was a strong positive correlation between mTORC1 activity and OPN expression in OSCC tissues and cell lines. Furthermore, mTOR complex 1 (mTORC1) enhanced OPN expression through up-regulation of ERRα. Therefore, OPN is a downstream target of mTORC1 and is crucial for OSCC development. mTORC1, ERRα, and OPN may be potential targets for treatment of OSCC with aberrant mTORC1 signaling.

Keywords: mTOR, ERRα, OPN, tumorigenesis, OSCC.