1. Academic Validation
  2. HPRT promotes proliferation and metastasis in head and neck squamous cell carcinoma through direct interaction with STAT3

HPRT promotes proliferation and metastasis in head and neck squamous cell carcinoma through direct interaction with STAT3

  • Exp Cell Res. 2021 Feb 1;399(1):112424. doi: 10.1016/j.yexcr.2020.112424.
Lin Wang 1 Yupu Wang 1 Nannan Han 1 Xu Wang 2 Min Ruan 3
Affiliations

Affiliations

  • 1 Department of Oral and Maxillofacial-Head and Neck Oncology, Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200011, China; Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai, 200011, China; National Clinical Research Center for Oral Disease, Shanghai, 200011, China.
  • 2 Department of Oral and Maxillofacial-Head and Neck Oncology, Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200011, China; Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai, 200011, China; National Clinical Research Center for Oral Disease, Shanghai, 200011, China. Electronic address: wangx312016@sh9hospital.org.cn.
  • 3 Department of Oral and Maxillofacial-Head and Neck Oncology, Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200011, China; Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai, 200011, China; National Clinical Research Center for Oral Disease, Shanghai, 200011, China. Electronic address: ruanm1740@sh9hospital.org.cn.
Abstract

Increasing effort has been put into finding novel molecular pathways to improve the efficiency of EGFR inhibitors against head and neck squamous cell Cancer (HNSCC). In this study, we performed data mining and bioinformatically analysed RNA-Seq data downloaded from TCGA and confirmed that higher expression of HPRT in HNSCC tissue was related to poor prognosis of patients. Then, we conducted in vitro and in vivo loss- and gain-of-function experiments to demonstrate the role of HPRT in HNSCC cell lines. Overexpression of HPRT increased the gene expression of epithelial mesenchymal transition markers via direct interaction with STAT3. Knocking down HPRT significantly decreased tumour growth and enhanced the Anticancer effect of EGFR inhibitors against HNSCC xenografts. In conclusion, HPRT is a binding partner of STAT3 that promotes EMT and proliferation. Our findings support HPRT as a promising prognostic indicator and potential therapeutic target for HNSCC.

Keywords

EGFR inhibitor; EMT; HNSCC; HPRT; STAT3.

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