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Abstract
BackgroundThe survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction.MethodsFour murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed.ResultsAll cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation.ConclusionsAs cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
Highlights
The survival of oral squamous cell carcinoma (OSCC) patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival
The induction of OSCC using a combination of a genetically engineered background and chemical carcinogen treatment will open up a door to understanding the exogenous and endogenous factors that contribute to OSCC in C57BL/6 mice [2]. miRNA disruption plays an important role in OSCC pathogenesis [6,7,8,9,10,11,12,13,14,15,16,17]
These cell lines and the linked immunocompetent animal model that we have established will facilitate the investigation of therapies that can be used to treat OSCC
Summary
The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. We have established miR-31 and miR-211 transgenic (Tg) mouse lines that have these transgenes overexpressed in the mouse basal keratinocytes [7, 8, 18] These mice show higher frequency and faster OSCC tumor induction following 4-nitroquinoline 1-oxide (4NQO) treatment [7, 8, 18, 19]. By means of these models, we have uncovered new suppressors that are targeted by these oncogenic miRNAs and unraveled the involvement of DNA defects and the enrichment of oxidative stress in OSCC progression. Due to the rapid tumor induction and fluorescent tumor labeling in these mice, the models have been used to enable new developments in image diagnosis [20]
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