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

• Published in: BMC cancer Vol. 19; no. 1; pp. 281 - 11
• Main Authors: Chen, Yi-Fen, Liu, Chung-Ji, Lin, Li-Han, Chou, Chung-Hsien, Yeh, Li-Yin, Lin, Shu-Chun, Chang, Kuo-Wei
• Format: Journal Article
• Language: English
• Published: London BioMed Central 29.03.2019; BioMed Central Ltd; BMC
• Subjects: 4-Nitroquinoline 1-oxide; Analysis; Animal models; Biomedical and Life Sciences; Biomedicine; Breast cancer; Cancer; Cancer metastasis; Cancer Research; Carcinogenesis; Carcinoma; Cell adhesion & migration; Cell and molecular biology; Cell growth; Cell lines; Cisplatin; Deoxyribonucleic acid; Dermis; DNA; DNA binding; Fluorescence; Genes; Genetic aspects; Genetic engineering; Genetically modified organisms; Head & neck cancer; Health Promotion and Disease Prevention; House mouse; Medicine/Public Health; Mesenchyme; Metastases; Metastasis; MicroRNA; miR-211; Missense mutation; Mouse; Mouth cancer; Oncology; Oral cancer; Oral carcinoma; Oxidative stress; p53 Protein; Pathogenesis; Patients; Research Article; Stem cells; Surgical Oncology; Tongue; Transgenic animals; Transgenic mice; Tumor cell lines; Tumor proteins; Tumorigenesis; Tumors; Xenografts; Oral carcinoma; microRNA; Tongue; Mouse; miR-211
• ISSN: 1471-2407; 1471-2407
• DOI: 10.1186/s12885-019-5486-7

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.