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Background  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. K14-EGFP- miR-211  transgenic mice also exhibit augmented potential for OSCC induction.    Methods  Four 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.    Results  All 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.    Conclusions  As 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.    Electronic supplementary material  The online version of this article (10.1186/s12885-019-5486-7) contains supplementary material, which is available to authorized users.

Establishing of mouse oral carcinoma cell lines derived from transgenic mice and their use as syngeneic tumorigenesis models