Potential Utility and Limitations of Thyroid Cancer Cell Lines As Models for Studying Thyroid Cancer

Overview

Journal Thyroid

Date 2009 Dec 17

PMID 20001716

Citations 38

Authors

Tania Pilli

Kanteti V Prasad

Shankar Jayarama

Furio Pacini

Bellur S Prabhakar

Affiliations

Soon will be listed here.

Abstract

Background: Tumor-derived cell lines are widely used to study the mechanisms involved in thyroid carcinogenesis but recent studies have reported redundancy among thyroid cancer cell lines and identification of some "thyroid cell lines" that are likely not of thyroid origin.

Summary: In this review, we have summarized the uses, the limitations, and the existing problems associated with the available follicular cell-derived thyroid cancer cell lines. There are some limitations to the use of cell lines as a model to "mimic" in vivo tumors. Based on the gene expression profiles of thyroid cell lines originating from tumors of different types it has become apparent that some of the cell lines are closely related to each other and to those of undifferentiated carcinomas. Further, many cell lines have lost the expression of thyroid-specific genes and have altered karyotypes, while they exhibit activation of several oncogenes (BRAF, v-raf murine sarcoma viral oncogene homolog B1; RAS, rat sarcoma; and RET/PTC, rearranged in transformation/papillary thyroid carcinoma) and inactivation of tumor suppressor gene (TP53) which is known to be important for thyroid tumorigenesis.

Conclusions: A careful selection of thyroid cancer cell lines that reflect the major characteristics of a particular type of thyroid cancer being investigated could be used as a good model system to analyze the signaling pathways that may be important in thyroid carcinogenesis. Further, the review of literature also suggests that some of the limitations can be overcome by using multiple cell lines derived from the same type of tumor.

Citing Articles

Recombinant Human TSH Fails to Induce the Proliferation and Migration of Papillary Thyroid Carcinoma Cell Lines.

Kalampounias G, Varemmenou A, Aronis C, Mamali I, Shaukat A, Chartoumpekis D Cancers (Basel). 2024; 16(14).

PMID: 39061242 PMC: 11275150. DOI: 10.3390/cancers16142604.

CD73 mitigates ZEB1 expression in papillary thyroid carcinoma.

Vedovatto S, Oliveira F, Pereira L, Scheffel T, Beckenkamp L, Bertoni A Cell Commun Signal. 2024; 22(1):145.

PMID: 38388432 PMC: 10882796. DOI: 10.1186/s12964-024-01522-z.

Thyroid-stimulating hormone receptor (TSHR) as a target for imaging differentiated thyroid cancer.

Gimblet G, Whitt J, Houson H, Lin D, Guenter R, Rao T Surgery. 2023; 175(1):199-206.

PMID: 37919223 PMC: 11744986. DOI: 10.1016/j.surg.2023.05.045.

Co-inhibition of glutaminolysis and one-carbon metabolism promotes ROS accumulation leading to enhancement of chemotherapeutic efficacy in anaplastic thyroid cancer.

Hwang Y, Yun H, Jeong J, Kim M, Joo S, Lee H Cell Death Dis. 2023; 14(8):515.

PMID: 37573361 PMC: 10423221. DOI: 10.1038/s41419-023-06041-2.

Targeting the inward rectifier potassium channel 5.1 in thyroid cancer: artificial intelligence-facilitated molecular docking for drug discovery.

Yang X, Wu Y, Xu S, Li H, Peng C, Cui X BMC Endocr Disord. 2023; 23(1):113.

PMID: 37208644 PMC: 10197823. DOI: 10.1186/s12902-023-01360-z.

References

Van Bokhoven A, Varella-Garcia M, Korch C, Johannes W, Smith E, Miller H . Molecular characterization of human prostate carcinoma cell lines. Prostate. 2003; 57(3):205-25. DOI: 10.1002/pros.10290. View

Nikiforova M, Nikiforov Y . Molecular genetics of thyroid cancer: implications for diagnosis, treatment and prognosis. Expert Rev Mol Diagn. 2007; 8(1):83-95. DOI: 10.1586/14737159.8.1.83. View

Lee J, Foukakis T, Hashemi J, Grimelius L, Heldin N, Wallin G . Molecular cytogenetic profiles of novel and established human anaplastic thyroid carcinoma models. Thyroid. 2007; 17(4):289-301. DOI: 10.1089/thy.2006.0246. View

van Bokhoven A, Varella-Garcia M, Korch C, Miller G . TSU-Pr1 and JCA-1 cells are derivatives of T24 bladder carcinoma cells and are not of prostatic origin. Cancer Res. 2001; 61(17):6340-4. View

Nikiforova M, Kimura E, Gandhi M, Biddinger P, Knauf J, Basolo F . BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab. 2003; 88(11):5399-404. DOI: 10.1210/jc.2003-030838. View

van Bokhoven A, Varella-Garcia M, Korch C, Hessels D, Miller G . Widely used prostate carcinoma cell lines share common origins. Prostate. 2001; 47(1):36-51. DOI: 10.1002/pros.1045. View

Riesco-Eizaguirre G, Gutierrez-Martinez P, Garcia-Cabezas M, Nistal M, Santisteban P . The oncogene BRAF V600E is associated with a high risk of recurrence and less differentiated papillary thyroid carcinoma due to the impairment of Na+/I- targeting to the membrane. Endocr Relat Cancer. 2006; 13(1):257-69. DOI: 10.1677/erc.1.01119. View

Liu D, Hu S, Hou P, Jiang D, Condouris S, Xing M . Suppression of BRAF/MEK/MAP kinase pathway restores expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutant. Clin Cancer Res. 2007; 13(4):1341-9. DOI: 10.1158/1078-0432.CCR-06-1753. View

Davies L, Welch H . Increasing incidence of thyroid cancer in the United States, 1973-2002. JAMA. 2006; 295(18):2164-7. DOI: 10.1001/jama.295.18.2164. View

10.

Yano Y, Kamma H, Matsumoto H, Fujiwara M, Bando H, Hara H . Growth suppression of thyroid cancer cells by adenylcyclase activator. Oncol Rep. 2007; 18(2):441-5. View

11.

Carlsson J, Nilsson K, Westermark B, Ponten J, Sundstrom C, Larsson E . Formation and growth of multicellular spheroids of human origin. Int J Cancer. 1983; 31(5):523-33. DOI: 10.1002/ijc.2910310502. View

12.

Challeton C, Branea F, Schlumberger M, Gaillard N, De Vathaire F, Badie C . Characterization and radiosensitivity at high or low dose rate of four cell lines derived from human thyroid tumors. Int J Radiat Oncol Biol Phys. 1997; 37(1):163-9. DOI: 10.1016/s0360-3016(96)00449-x. View

13.

Wyllie F, Haughton M, Blaydes J, Schlumberger M, Wynford-Thomas D . Evasion of p53-mediated growth control occurs by three alternative mechanisms in transformed thyroid epithelial cells. Oncogene. 1995; 10(1):49-59. View

14.

Roque L, Nunes V, Ribeiro C, Martins C, Soares J . Karyotypic characterization of papillary thyroid carcinomas. Cancer. 2001; 92(10):2529-38. DOI: 10.1002/1097-0142(20011115)92:10<2529::aid-cncr1604>3.0.co;2-m. View

15.

Nikolova D, Zembutsu H, Sechanov T, Vidinov K, Kee L, Ivanova R . Genome-wide gene expression profiles of thyroid carcinoma: Identification of molecular targets for treatment of thyroid carcinoma. Oncol Rep. 2008; 20(1):105-21. View

16.

Alvarez-Nunez F, Bussaglia E, Mauricio D, Ybarra J, Vilar M, Lerma E . PTEN promoter methylation in sporadic thyroid carcinomas. Thyroid. 2006; 16(1):17-23. DOI: 10.1089/thy.2006.16.17. View

17.

Xing M, Cohen Y, Mambo E, Tallini G, Udelsman R, Ladenson P . Early occurrence of RASSF1A hypermethylation and its mutual exclusion with BRAF mutation in thyroid tumorigenesis. Cancer Res. 2004; 64(5):1664-8. DOI: 10.1158/0008-5472.can-03-3242. View

18.

Carrasco N . Iodide transport in the thyroid gland. Biochim Biophys Acta. 1993; 1154(1):65-82. DOI: 10.1016/0304-4157(93)90017-i. View

19.

Fagin J, Matsuo K, Karmakar A, Chen D, Tang S, Koeffler H . High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas. J Clin Invest. 1993; 91(1):179-84. PMC: 330012. DOI: 10.1172/JCI116168. View

20.

Bird A . The relationship of DNA methylation to cancer. Cancer Surv. 1996; 28:87-101. View