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.

视黄醇结合蛋白1（RBP1）参与多种生理功能，包括代谢和视黄醇运输的调节。研究表明，它在几种类型的癌症的发病机理中起着重要作用。但是，RBP1的作用及其与自噬在口腔鳞状细胞癌（OSCC）发病机理中的关系仍然未知。在这项研究中，通过基于iTRAQ的蛋白质组学分析和二维LC-MS / MS，与正常组织相比，RBP1被确定为OSCC样品中上调幅度最大2倍以上的DEP。RBP1的过表达与OSCC的恶性表型（分化，TNM分期和淋巴结转移）显着相关。体外实验表明，与对照组相比，OSCC组织和细胞系中的RBP1显着增加。RBP1过表达促进细胞生长，迁移和侵袭OSCC细胞。RBP1沉默抑制异种移植小鼠中的肿瘤形成。我们进一步证明，RBP1-CKAP4轴是OSCC自噬机制的关键调节剂，自噬的失活拯救了RBP1-CKAP4介导的OSCC细胞恶性生物学行为。总体而言，RBP1-CKAP4在主要致癌特征和自噬诱导之间提供了机理联系，这可能提供了潜在的治疗靶点，值得进一步研究OSCC的治疗方法。RBP1沉默抑制异种移植小鼠中的肿瘤形成。我们进一步证明，RBP1-CKAP4轴是OSCC自噬机制的关键调节剂，自噬的失活拯救了RBP1-CKAP4介导的OSCC细胞恶性生物学行为。总体而言，RBP1-CKAP4在主要致癌特征和自噬诱导之间提供了机理联系，这可能提供了潜在的治疗靶点，值得进一步研究OSCC的治疗方法。RBP1沉默抑制异种移植小鼠中的肿瘤形成。我们进一步证明，RBP1-CKAP4轴是OSCC自噬机制的关键调节剂，自噬的失活拯救了RBP1-CKAP4介导的OSCC细胞恶性生物学行为。总体而言，RBP1-CKAP4在主要致癌特征和自噬诱导之间提供了机理联系，这可能提供了潜在的治疗靶点，值得进一步研究OSCC的治疗方法。