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  • Establishment of OC3 oral carcinoma cell line and identification of NF-kappa B activation responses to areca nut extract.

Establishment of OC3 oral carcinoma cell line and identification of NF-kappa B activation responses to areca nut extract.

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology (2004-01-15)
Shu-Chun Lin, Chung-Ji Liu, Chun-Po Chiu, Shun-Ming Chang, Suu-Yi Lu, Yann-Jang Chen
ABSTRACT

Cell lines derived from oral squamous cell carcinoma (OSCC) exposed to variable etiological factors can bestow advantages in understanding the molecular and cellular alterations pertaining to environmental impacts. Most OSCC cell lines have been established from smoker patients or areca chewing/smoker patients, carrying the genomic alterations in p53. A new cell line, oral carcinoma 3 (OC3), was established from an OSCC in a long-term areca (betel) chewer who does not smoke. Cellular and molecular features of OC3 were determined by variable assays. The cultured monolayer cells were mainly polygonal and had the expression of cytokeratin 14. The chromosomal analysis using comparative genomic hybridization has revealed the gain in chromosomes 1q, 5q, and 8q, the loss in 4q, 6p, and 8p as well as the gain of entire chromosome 20. Loss of heterozygosity and instability in multiple microsatellite markers in chromosome 4q were also noted. OC3 cells bear wild-type p53 coding sequence and have a high level of p53 expression. Its p21 expression was similar to that in normal human oral keratinocyte (NHOK). Interestingly, activation of nuclear factor kappa B (NF-kappa B) in OC3 cells following the treatment of areca nut extract was observed. OC3 cell line could be valuable in understanding the genetic impairments and phenotypic changes associated with areca in oral keratinocyte.

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OECM-1 Human Oral Squamous Carcinoma Cell Line, OECM-1 human oral squamous carcinoma cell line is suitable for studies of cancer cell signaling, epithelial-mesenchymal transition (EMT), metastasis, invasion, and cancer cell stemness.