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Establishment of a Tongue Squamous Cell Carcinoma Cell Line from Indian Gutka Chewer

DOI: 10.1155/2014/286013

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Abstract:

CD cell line has been established from a poorly differentiated squamous cell carcinoma of tongue. This is a first ever cell line established from an Indian gutka chewer. Cell line was characterized for morphology, ultrastructure, doubling time, expression of epithelial markers, DNA content, karyotyping, STR markers, p53 mutations, HPV status, and tumorigenicity in SCID mice with all-trans-retinoic acid and cisplatin. The epithelial phenotype of the cell line was confirmed with surface markers and ultrastructure. The cell line is hyperploid with chromosomal alterations like gain of chromosomes 8q and 11q. CD cell line shows a unique pattern on STR genotyping and carries a missense mutation R273C in TP53. It does not show genomic integration of HPV. The cells are nontumorigenic to SCID mice and show growth inhibition upon treatment with cisplatin, and all-trans-retinoic acid. This cell line may be useful as an in vitro tool to understand the molecular changes associated with oral cancers. 1. Introduction Cancer of oral cavity is the third most common cancer in India (http://globocan.iarc.fr/Pages/online.aspx). The important risk factors identified so far are tobacco use and alcohol consumption, which seem to have a synergistic effect. Statistics for head and neck squamous cell cancers (HNSCCs) throughout the world show these cancers to be prevalent in areas where consumption of tobacco and alcohol is high [1]. The process of oral carcinogenesis is multifactorial with interplay of various environmental factors. Though treatment modalities have shown an advancement, the survival rates of oral cancer patients have not improved markedly over the past few decades [2]. Tumor derived cell lines form a useful resource as model systems with reflections of the original tumors [3]. Therefore, development of cell lines from tumor tissues will aid in understanding the events associated with development of cancer. Moreover, cell lines are required to study the effects of various known and novel drug formulations and help in studying future treatment strategies. In spite of these advantages, there are very few cell lines developed from Indian oral cancer patients [4–6]. We have established an oral cancer cell line CD from a young gutka chewer. Gutka is a dry mixture of areca nut, catechu, and slaked lime with tobacco. Due to its easy availability and low cost, it has become popular chewing substitute in young Indian tobacco habitués. Use of gutka has been strongly implicated in increased incidence of oral submucous fibrosis, a precancerous lesion, which has a high rate

References

[1]  S. S. Hecht, “Tobacco carcinogens, their biomarkers and tobacco-induced cancer,” Nature Reviews Cancer, vol. 3, no. 10, pp. 733–744, 2003.
[2]  C. R. Leemans, B. J. M. Braakhuis, and R. H. Brakenhoff, “The molecular biology of head and neck cancer,” Nature Reviews Cancer, vol. 11, no. 1, pp. 9–22, 2011.
[3]  J. S. White, J. L. Weissfeld, C. C. R. Ragin et al., “The influence of clinical and demographic risk factors on the establishment of head and neck squamous cell carcinoma cell lines,” Oral Oncology, vol. 43, no. 7, pp. 701–712, 2007.
[4]  J. Kaur and R. Ralhan, “Establishment and characterization of a cell line from smokeless tobacco associated oral squamous cell carcinoma,” Oral Oncology, vol. 39, no. 8, pp. 806–820, 2003.
[5]  R. Mulherkar, A. P. Goud, A. S. Wagle et al., “Establishment of a human squamous cell carcinoma cell line of the upper aero-digestive tract,” Cancer Letters, vol. 118, no. 1, pp. 115–121, 1997.
[6]  R. J. Tatake, N. Rajaram, R. N. Damle, B. Balsara, A. N. Bhisey, and S. G. Gangal, “Establishment and characterization of four new squamous cell carcinoma cell lines derived from oral tumors,” Journal of Cancer Research and Clinical Oncology, vol. 116, no. 2, pp. 179–186, 1990.
[7]  D. S. Aruna, K. V. V. Prasad, G. R. Shavi, J. Ariga, G. Rajesh, and M. Krishna, “Retrospective study on risk habits among oral cancer patients in karnataka cancer therapy and research institute, hubli, India,” Asian Pacific Journal of Cancer Prevention, vol. 12, no. 6, pp. 1561–1566, 2011.
[8]  P. C. Gupta, “Mouth cancer in India: a new epidemic?” Journal of the Indian Medical Association, vol. 97, no. 9, pp. 370–373, 1999.
[9]  U. Nair, H. Bartsch, and J. Nair, “Alert for an epidemic of oral cancer due to use of the betel quid substitutes gutkha and pan masala: a review of agents and causative mechanisms,” Mutagenesis, vol. 19, no. 4, pp. 251–262, 2004.
[10]  J. Wulong, L. Zhou, Z. Xiaojian, T. Jie, and G. Huilin, “Establishment of a highly metastatic tongue squamous cell carcinoma cell line from New Zealand White rabbit,” Archives of Oral Biology, vol. 53, no. 11, pp. 1084–1090, 2008.
[11]  S. Ambatipudi, M. Gerstung, R. Gowda et al., “Genomic profiling of advanced-stage oral cancers reveals chromosome 11q alterations as markers of poor clinical outcome,” PLoS ONE, vol. 6, no. 2, Article ID e17250, 2011.
[12]  S. Pathare, A. A. Sch?ffer, N. Beerenwinkel, and M. Mahimkar, “Construction of oncogenetic tree models reveals multiple pathways of oral cancer progression,” International Journal of Cancer, vol. 124, no. 12, pp. 2864–2871, 2009.
[13]  Y. Liu and W. F. Bodmer, “Analysis of P53 mutations and their expression in 56 colorectal cancer cell lines,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 4, pp. 976–981, 2006.
[14]  T. Mosmann, “Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays,” Journal of Immunological Methods, vol. 65, no. 1-2, pp. 55–63, 1983.
[15]  E. J. Lee, J. Kim, S. A. Lee et al., “Characterization of newly established oral cancer cell lines derived from six squamous cell carcinoma and two mucoepidermoid carcinoma cells,” Experimental and Molecular Medicine, vol. 37, no. 5, pp. 379–390, 2005.
[16]  G. E. Moore, S. B. Merrick, L. K. Woods, and N. M. Arabasz, “A human squamous cell carcinoma cell line,” Cancer Research, vol. 35, no. 10, pp. 2684–2688, 1975.
[17]  H. T. Rupniak, C. Rowlatt, and E. B. Lane, “Characteristics of four new human cell lines derived from squamous cell carcinomas of the head and neck,” Journal of the National Cancer Institute, vol. 75, no. 4, pp. 621–635, 1985.
[18]  S. Hamid, K. P. Lim, R. B. Zain et al., “Establishment and characterization of Asian oral cancer cell lines as in vitro models to study a disease prevalent in Asia,” International Journal of Molecular Medicine, vol. 19, no. 3, pp. 453–460, 2007.
[19]  K. D. Hunter, E. K. Parkinson, and P. R. Harrison, “Profiling early head and neck cancer,” Nature Reviews Cancer, vol. 5, no. 2, pp. 127–135, 2005.
[20]  M. L. Gillison, W. M. Koch, and K. V. Shah, “Human papillomavirus in head and neck squamous cell carcinoma: are some head and neck cancers a sexually transmitted disease?” Current Opinion in Oncology, vol. 11, no. 3, pp. 191–199, 1999.
[21]  H. Alam, S. T. Kundu, S. N. Dalal, and M. M. Vaidya, “Loss of keratins 8 and 18 leads to alterations in α6β4-integrin-mediated signalling and decreased neoplastic progression in an oral-tumour-derived cell line,” Journal of Cell Science, vol. 124, no. 12, pp. 2096–2106, 2011.
[22]  M. M. Vaidya, A. M. Borges, S. A. Pradhan, and A. N. Bhisey, “Cytokeratin expression in squamous cell carcinomas of the tongue and alveolar mucosa,” European Journal of Cancer Part B: Oral Oncology, vol. 32, no. 5, pp. 333–336, 1996.
[23]  C. L. Martin, S. C. Reshmi, T. Ried et al., “Chromosomal imbalances in oral squamous cell carcinoma: examination of 31 cell lines and review of the literature,” Oral Oncology, vol. 44, no. 4, pp. 369–382, 2008.
[24]  S. M. Gollin, “Chromosomal alterations in squamous cell carcinomas of the head and neck: window to the biology of disease,” Head Neck, vol. 23, no. 3, pp. 238–253, 2001.
[25]  M. L. Gillison, “Human papillomavirus-associated head and neck cancer is a distinct epidemiologic, clinical, and molecular entity,” Seminars in Oncology, vol. 31, no. 6, pp. 744–754, 2004.
[26]  J. P. Klussmann, J. J. Mooren, M. Lehnen et al., “Genetic signatures of HPV-related and unrelated oropharyngeal carcinoma and their prognostic implications,” Clinical Cancer Research, vol. 15, no. 5, pp. 1779–1786, 2009.
[27]  C. Fakhry, W. H. Westra, S. Li et al., “Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial,” Journal of the National Cancer Institute, vol. 100, no. 4, pp. 261–269, 2008.
[28]  D. Rischin, R. J. Young, R. Fisher et al., “Prognostic significance of p16INK4Aand human papillomavirus in patients with oropharyngeal cancer treated on TROG 02.02 phase III trial,” Journal of Clinical Oncology, vol. 28, no. 27, pp. 4142–4148, 2010.
[29]  K. K. Ang, J. Harris, R. Wheeler et al., “Human papillomavirus and survival of patients with oropharyngeal cancer,” The New England Journal of Medicine, vol. 363, no. 1, pp. 24–35, 2010.
[30]  P. K. Ha, S. I. Pai, W. H. Westra et al., “Real-time quantitative PCR demonstrates low prevalence of human papillomavirus type 16 in premalignant and malignant lesions of the oral cavity,” Clinical Cancer Research, vol. 8, no. 5, pp. 1203–1209, 2002.
[31]  J. P. Klussmann, S. J. Weissenborn, and U. Wieland, “Prevalence, distribution, and viral load of human papillomavirus 16 DNA in tonsillar carcinomas,” Cancer, vol. 92, no. 11, pp. 2875–2884, 2001.
[32]  M. L. Gillison, W. M. Koch, R. B. Capone et al., “Evidence for a causal association between human papillomavirus and a subset of head and neck cancers,” Journal of the National Cancer Institute, vol. 92, no. 9, pp. 709–720, 2000.
[33]  L.-L. Hsieh, P.-F. Wang, I.-H. Chen et al., “Characteristics of mutations in the p53 gene in oral squamous cell carcinoma associated with betel quid chewing and cigarette smoking in Taiwanese,” Carcinogenesis, vol. 22, no. 9, pp. 1497–1503, 2001.
[34]  S. Kalyankrishna and J. R. Grandis, “Epidermal growth factor receptor biology in head and neck cancer,” Journal of Clinical Oncology, vol. 24, no. 17, pp. 2666–2672, 2006.
[35]  J. H. Ludes-Meyers, M. A. Subler, C. V. Shivakumar et al., “Transcriptional activation of the human epidermal growth factor receptor promoter by human p53,” Molecular and Cellular Biology, vol. 16, no. 11, pp. 6009–6019, 1996.
[36]  Y. Hiraishi, T. Wada, K. Nakatani et al., “EGFR inhibitor enhances cisplatin sensitivity of oral squamous cell carcinoma cell lines,” Pathology and Oncology Research, vol. 14, no. 1, pp. 39–43, 2008.

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