Abstract
Retinol-binding protein 1 (RBP1) is involved in several physiological functions, including the regulation of the metabolism and retinol transport. Studies have shown that it plays an important role in the pathogenesis of several types of cancer. However, the role of RBP1 and its correlation with autophagy in oral squamous cell carcinoma (OSCC) pathogenesis remain unknown. In this study, RBP1 was identified as the most significantly upregulated DEPs with a >2-fold change in OSCC samples when compared to normal tissues through iTRAQ-based proteomics analysis coupled with 2D LC–MS/MS. RBP1 overexpression was significantly associated with malignant phenotypes (differentiation, TNM stage, and lymphatic metastasis) of OSCC. In vitro experiments demonstrated that RBP1 was significantly increased in OSCC tissues and cell lines compared with control group. RBP1 overexpression promoted cell growth, migration, and invasion of OSCC cells. Silencing of RBP1 suppressed tumor formation in xenografted mice. We further demonstrated that the RBP1–CKAP4 axis was a critical regulator of the autophagic machinery in OSCC, inactivation of autophagy rescued the RBP1–CKAP4-mediated malignant biological behaviors of OSCC cells. Overall, a mechanistic link was provided by RBP1–CKAP4 between primary oncogenic features and the induction of autophagy, which may provide a potential therapeutic target that warrants further investigation for treatment of OSCC.
Highlights
Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors and accounts for ~90% of oral cancers[1,2]
We validated the result that Retinol-binding protein 1 (RBP1) was increased in OSCC compared with normal tissues using quantitative real-time PCR analysis (Fig. 1e)
We have provided evidence for RBP1 as a biomarker in OSCC, and its novel role as an inducer of autophagy that further promotes in vitro and in vivo tumor cell growth via interaction with CKAP4 (Supplementary Fig. 2)
Summary
Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors and accounts for ~90% of oral cancers[1,2]. Mortality and recurrence rate of OSCC has not decreased significantly during the past 30 years despite advances in therapeutic strategies and 5‐year survival rate remains
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