Oral carcinoma develops from squamous epithelial cells by the acquisition of multiple (epi) genetic alterations that target different genes and molecular pathways. Herein, we performed a comprehensive genomic and epigenetic characterization of the HSC-3 cell line through karyotyping, multicolor fluorescence in situ hybridization, array comparative genomic hybridization, and methylation-specific multiplex ligation-dependent probe amplification. HSC-3 turned out to be a near-triploid cell line with a modal number of 61 chromosomes. Banding and molecular cytogenetic analyses revealed that nonrandom gains of chromosomal segments occurred more frequently than losses. Overall, gains of chromosome 1, 3q, 5p, 7p, 8q, 9q, 10, 11p, 11q13, 12, 13, 14, 17, 18p, 20, Yp, and Xq were observed. The largest region affected by copy number loss was observed at chromosome 18q. Several of the observed genomic imbalances and their mapped genes were already associated with oral carcinoma and/or adverse prognosis, invasion, and metastasis in cancer. The most common rearrangements observed were translocations in the centromeric/near-centromeric regions. RARB, ESR1, and CADM1 genes were methylated and showed copy number losses, whereas TP73 and GATA5 presented with methylation and copy number gains. Thus, the current study presents a comprehensive characterization of the HSC-3 cell line; the use of this cell line may contribute to enriching the resources available for oral cancer research, especially for the testing of therapeutic agents.
Keywords: HSC-3; chromosomal rearrangements; copy number alterations; methylation; oral cavity cell lines; translocation.