Abstract
Objective GIT1 is identified as a novel tumor oncogene in breast cancer. In this article, we aimed to explore the role of GIT1 in the progression of head and neck squamous cell carcinoma (HNSCC). Methods GIT1 expression in HNSCC was detected by RT-qPCR, immunohistochemistry assay, and Western blot. HNSCC cell proliferation, migration, and invasion were examined by CCK-8 assay, Wound healing assay, and Transwell assay, respectively. Cell apoptosis was detected by flow cytometric analysis. Results In our study, GIT1 was notably upregulated in HNSCC tissues and cells. Moreover, GIT1 expression level had positive corelation with pathological grade and nodal status of HNSCC. Functional experiments showed that knockdown of GIT1 restrained HNSCC proliferation, invasion, migration, and EMT and facilitated cell apoptosis. Furthermore, GIT1 knockdown was found to restrain HNSCC tumor growth and lung metastasis. Additionally, PI3K/AKT/mTOR signal pathway inhibitors suppressed the effect of GIT1 on HNSCC cell progression. Conclusion GIT1 was upregulated in HNSCC and facilitated HNSCC cell progression by inducing PI3K/AKT/mTOR signal pathway. Therefore, we suggested that GIT1 might be a potential target for HNSCC treatment.
Highlights
Head and neck squamous cell carcinoma (HNSCC) is a type of malignant tumor originated from different organs of the head and neck [1, 2]
We found that G-protein-coupled receptor kinase-interacting protein 1 (GIT1) facilitated HNSCC cell progression through PI3K/ AKT/mTOR pathway
The GEPIA dataset displayed that there were no significant differences between GIT1 expression and the overall survival (OS) probability (p = 0:1, Figure 1(e)), while high GIT1 expression had a significant low disease-free survival (DFS) probability (p = 0:025, Figure 1(f))
Summary
Head and neck squamous cell carcinoma (HNSCC) is a type of malignant tumor originated from different organs of the head and neck [1, 2]. The usual treatment for HNSCC patients is chemotherapy or radiotherapy [4, 5]. Despite extensive basic research and available options of clinical treatments, the 5-year survival rate of HNSCC patients is less than 50% [6]. G-protein-coupled receptor kinase-interacting protein 1 (GIT1) is a cellular hetero shuttle protein that can interact with various protein kinases to regulate the overall cellular function [7]. GIT1 has been reported to promote bone regeneration by regulating ERK/NRF2 pathways in macrophages [10]. GIT1 promoted tumor progression by activating ERK/MMP9
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