BST2 regulated by the transcription factor STAT1 can promote metastasis, invasion and proliferation of oral squamous cell carcinoma via the AKT/ERK1/2 signaling pathway

Abstract

Oral squamous cell carcinoma (OSCC) is one of the main types of head and neck squamous cell carcinoma. Although progress has been made in treating OSCC, it remains a threat to human health, and novel therapeutic strategies are needed to extend the lifespan of patients with OSCC. The present study, evaluated whether bone marrow stromal antigen 2 (BST2) and STAT1 were potential therapeutic targets in OSCC. Small interfering RNA (siRNA) or overexpression plasmids were used to regulate BST2 or STAT1 expression. Western blotting and reverse transcription-quantitative PCR were performed to assess changes in the protein and mRNA expression levels of signaling pathway components. The effects of BST2 and STAT1 expression changes on the migration, invasion and proliferation of OSCC cells were assessed using the scratch test assay, Transwell assay and colony formation assay in vitro, respectively. Cell-derived xenograft models were used to evaluate the impact of BST2 and STAT1 on the occurrence and development of OSCC in vivo. Finally, it was demonstrated that BST2 expression was significantly upregulated in OSCC. Furthermore, it was demonstrated that high expression of BST2 in OSCC contributed to the metastasis, invasion and proliferation of OSCC cells. Moreover, it was demonstrated that the promoter region of BST2 was regulated by the transcription factor STAT1, and that the STAT1/BST2 axis could affect the behavior of OSCC via the AKT/ERK1/2 signaling pathway. In vivo studies also demonstrated that STAT1 downregulation inhibited OSCC growth by down-regulating BST2 expression via the AKT/ERK1/2 signaling pathway.

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

“…FEN1 may directly or indirectly regulate HLA-DR and PD-L1 in OSCC via the IFN-γ/JAK/STAT1 pathway ( Wang et al, 2023 ). Shan et al reported that the downregulation of STAT1/BST2 axis inhibited OSCC cell growth through the AKT/ERK1/2 signaling pathway ( Shan et al, 2023 ). Overall, above results demonstrate that the JAK/STAT signaling pathway is a potential molecular target and biomarker for OSCC.…”

Uncovering periodontitis-associated markers through the aggregation of transcriptomics information from diverse sources

“…Zhou et al found that CENPU was a key gene in the development of LUAD, closely associated with the infiltration of various immune cells ( Zhou et al, 2021 ). Shan et al found that BST2 contributes to the promotion of metastasis, invasion and proliferation of oral squamous cell carcinoma ( Shan et al, 2023 ). Through the above core gene-associated lncRNAs, it has been shown that the above lncRNAs were related to the value-added and differentiation regulation of cancer cells, and LINC00174 is related to immune regulation.…”

The Role of IL-17 in the Pathogenesis of Oral Squamous Cell Carcinoma

“…Due to the impact on mRNA metabolism, IL-17 is able to perform its activity synergistically with other cytokines and activates diverse signaling pathways. Interleukin-17 and TNF-α synergistically activate NF-κB, a transcriptional factor with known roles in the promotion of inflammation and OSCC progression [ 117 , 118 , 119 ]. Interleukin-17 signals cooperatively with the IFN-γ enhances activation of STAT1, a molecule involved in signaling pathways important for OSCC growth and metastasis [ 120 , 121 ].…”