Thyroid cancer is a malignant neoplasm originated from thyroid cells. It can be classified into papillary carcinomas (PTCs) and anaplastic carcinomas (ATCs). Although ATCs are in an very aggressive status and cause more death than PTCs, their difference is poorly understood at molecular level. In this study, we focus on the transcriptome difference among PTCs, ATCs and normal tissue from a published dataset including 45 normal tissues, 49 PTCs and 11 ATCs, by applying a machine learning method, maximum relevance minimum redundancy, and identified 9 genes (BCL2, MRPS31, ID4, RASAL2, DLG2, MY01B, ZBTB5, PRKCQ and PPP6C) and 1 miscRNA (miscellaneous RNA, LOC646736) as important candidates involved in the progression of thyroid cancer. We further identified the protein-protein interaction (PPI) sub network from the shortest paths among the 9 genes in a PPI network constructed based on STRING database. Our results may provide insights to the molecular mechanism of the progression of thyroid cancer.
References
[1]
Ain KB (1999) Anaplastic thyroid carcinoma: A therapeutic challenge. Seminars in Surgical Oncology 16: 64–69. doi: 10.1002/(sici)1098-2388(199901/02)16:1<64::aid-ssu10>3.0.co;2-u
[2]
Smallridge RC, Marlow LA, Copland JA (2009) Anaplastic thyroid cancer: molecular pathogenesis and emerging therapies. Endocrine-Related Cancer 16: 17–44. doi: 10.1677/erc-08-0154
[3]
Montero-Conde C, Martin-Campos JM, Lerma E, Gimenez G, Martinez-Guitarte JL, et al. (2008) Molecular profiling related to poor prognosis in thyroid carcinoma. Combining gene expression data and biological information. Oncogene 27: 1554–1561. doi: 10.1038/sj.onc.1210792
[4]
Salvatore G, Nappi TC, Salerno P, Jiang Y, Garbi C, et al. (2007) A cell proliferation and chromosomal instability signature in anaplastic thyroid carcinoma. Cancer Research 67: 10148–10158. doi: 10.1158/0008-5472.can-07-1887
[5]
Hebrant A, Dom G, Dewaele M, Andry G, Tresallet C, et al. (2012) mRNA Expression in Papillary and Anaplastic Thyroid Carcinoma: Molecular Anatomy of a Killing Switch. Plos One 7.
[6]
Li B-Q, Huang T, Liu L, Cai Y-D, Chou K-C (2012) Identification of Colorectal Cancer Related Genes with mRMR and Shortest Path in Protein-Protein Interaction Network. Plos One 7.
[7]
Szklarczyk D, Franceschini A, Kuhn M, Simonovic M, Roth A, et al. (2011) The STRING database in 2011: functional interaction networks of proteins, globally integrated and scored. Nucleic Acids Research 39: D561–D568. doi: 10.1093/nar/gkq973
[8]
Csardi G, Nepusz T (2006) The igraph software package for complex network research. InterJounal Complex Systems: 1695.
[9]
Peng HC, Long FH, Ding C (2005) Feature selection based on mutual information: Criteria of max-dependency, max-relevance, and min-redundancy. Ieee Transactions on Pattern Analysis and Machine Intelligence 27: 1226–1238. doi: 10.1109/tpami.2005.159
[10]
Friedman JH, Baskett F, Shustek LJ (1975) An Algorithm for Finding Nearest Neighbors. Computers, IEEE Transactions on C-24: 1000–1006. doi: 10.1109/t-c.1975.224110
[11]
Chou K-C, Shen H-B (2006) Predicting eukaryotic protein subcellular location by fusing optimized evidence-theoretic K-Nearest Neighbor classifiers. Journal of Proteome Research 5: 1888–1897. doi: 10.1021/pr060167c
[12]
Chou K-C (2011) Some remarks on protein attribute prediction and pseudo amino acid composition. Journal of Theoretical Biology 273: 236–247. doi: 10.1016/j.jtbi.2010.12.024
[13]
Li B-Q, Hu L-L, Chen L, Feng K-Y, Cai Y-D, et al. (2012) Prediction of Protein Domain with mRMR Feature Selection and Analysis. PLoS ONE 7: e39308. doi: 10.1371/journal.pone.0039308
[14]
Ambroise C, McLachlan GJ (2002) Selection bias in gene extraction on the basis of microarray gene-expression data. Proceedings of the National Academy of Sciences of the United States of America 99: 6562–6566. doi: 10.1073/pnas.102102699
[15]
Kohavi R (1995) A study of cross-validation and bootstrap for accuracy estimation and model selection. Proceedings of the 14th international joint conference on Artificial intelligence- Volume 2. Montreal, Quebec, Canada: Morgan Kaufmann Publishers Inc. pp. 1137–1143.
[16]
Dijkstra E (1959) A note on two problems in connection with graphs. Numerische Mathematik 1: 269–271. doi: 10.1007/bf01386390
[17]
Huang DW, Sherman BT, Lempicki RA (2009) Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nature Protocols 4: 44–57. doi: 10.1038/nprot.2008.211
[18]
Cronin SJF, Penninger JM (2007) From T-cell activation signals to signaling control of anti-cancer immunity. Immunological Reviews 220: 151–168. doi: 10.1111/j.1600-065x.2007.00570.x
[19]
Heubner M, Wimberger P, Otterbach F, Kasimir-Bauer S, Siffert W, et al. (2009) Association of the AA genotype of the BCL2 (-938C>A) promoter polymorphism with better survival in ovarian cancer. Int J Biol Markers 24: 223–229.
[20]
Bachmann HS, Otterbach F, Callies R, Nuckel H, Bau M, et al. (2007) The AA genotype of the regulatory BCL2 promoter polymorphism (938C>A) is associated with a favorable outcome in lymph node negative invasive breast cancer patients. Clin Cancer Res 13: 5790–5797. doi: 10.1158/1078-0432.ccr-06-2673
[21]
Bachmann HS, Heukamp LC, Schmitz KJ, Hilburn CF, Kahl P, et al. (2011) Regulatory BCL2 promoter polymorphism (-938C>A) is associated with adverse outcome in patients with prostate carcinoma. Int J Cancer 129: 2390–2399. doi: 10.1002/ijc.25904
[22]
Rossi D, Rasi S, Capello D, Gaidano G (2008) Prognostic assessment of BCL2-938C>A polymorphism in chronic lymphocytic leukemia. Blood 111: 466–468. doi: 10.1182/blood-2007-08-106823
[23]
Aksoy M, Giles Y, Kapran Y, Terzioglu T, Tezelman S (2005) Expression of bcl-2 in papillary thyroid cancers and its prognostic value. Acta Chir Belg 105: 644–648.
[24]
Eun YG, Hong IK, Kim SK, Park HK, Kwon S, et al. (2011) A Polymorphism (rs1801018, Thr7Thr) of BCL2 is Associated with Papillary Thyroid Cancer in Korean Population. Clin Exp Otorhinolaryngol 4: 149–154. doi: 10.3342/ceo.2011.4.3.149
[25]
Noetzel E, Veeck J, Niederacher D, Galm O, Horn F, et al. (2008) Promoter methylation-associated loss of ID4 expression is a marker of tumour recurrence in human breast cancer. BMC Cancer 8: 154. doi: 10.1186/1471-2407-8-154
[26]
Deleu S, Savonet V, Behrends J, Dumont JE, Maenhaut C (2002) Study of gene expression in thyrotropin-stimulated thyroid cells by cDNA expression array: ID3 transcription modulating factor as an early response protein and tumor marker in thyroid carcinomas. Exp Cell Res 279: 62–70. doi: 10.1006/excr.2002.5589
[27]
Kebebew E, Peng M, Treseler PA, Clark OH, Duh QY, et al. (2004) Id1 gene expression is up-regulated in hyperplastic and neoplastic thyroid tissue and regulates growth and differentiation in thyroid cancer cells. J Clin Endocrinol Metab 89: 6105–6111. doi: 10.1210/jc.2004-1234
[28]
Rigolet M, Rich T, Gross-Morand MS, Molina-Gomes D, Viegas-Pequignot E, et al. (1998) cDNA cloning, tissue distribution and chromosomal localization of the human ID4 gene. DNA Res 5: 309–313. doi: 10.1093/dnares/5.5.309
[29]
Chen GG, Vlantis AC, Zeng Q, van Hasselt CA (2008) Regulation of cell growth by estrogen signaling and potential targets in thyroid cancer. Curr Cancer Drug Targets 8: 367–377. doi: 10.2174/156800908785133150
[30]
Fujimoto J, Hirose R, Ichigo S, Sakaguchi H, Tamaya T (1998) DNA polymorphism in B-domain of the estrogen receptor-alpha among Japanese women. Steroids 63: 146–148. doi: 10.1016/s0039-128x(97)00157-8
[31]
Lehrer SP, Schmutzler RK, Rabin JM, Schachter BS (1993) An estrogen receptor genetic polymorphism and a history of spontaneous abortion—correlation in women with estrogen receptor positive breast cancer but not in women with estrogen receptor negative breast cancer or in women without cancer. Breast Cancer Res Treat 26: 175–180. doi: 10.1007/bf00689690
[32]
Massart F, Becherini L, Gennari L, Facchini V, Genazzani AR, et al. (2001) Genotype distribution of estrogen receptor-alpha gene polymorphisms in Italian women with surgical uterine leiomyomas. Fertil Steril 75: 567–570. doi: 10.1016/s0015-0282(00)01760-x
[33]
Rebai M, Kallel I, Charfeddine S, Hamza F, Guermazi F, et al. (2009) Association of polymorphisms in estrogen and thyroid hormone receptors with thyroid cancer risk. J Recept Signal Transduct Res 29: 113–118. doi: 10.1080/10799890902845682
[34]
Leeman-Neill RJ, Brenner AV, Little MP, Bogdanova TI, Hatch M, et al. (2013) RET/PTC and PAX8/PPARgamma chromosomal rearrangements in post-Chernobyl thyroid cancer and their association with iodine-131 radiation dose and other characteristics. Cancer 119: 1792–1799. doi: 10.1002/cncr.27893
[35]
McIver B, Grebe SK, Eberhardt NL (2004) The PAX8/PPAR gamma fusion oncogene as a potential therapeutic target in follicular thyroid carcinoma. Curr Drug Targets Immune Endocr Metabol Disord 4: 221–234. doi: 10.2174/1568008043339802
[36]
Eberhardt NL, Grebe SK, McIver B, Reddi HV (2010) The role of the PAX8/PPARgamma fusion oncogene in the pathogenesis of follicular thyroid cancer. Mol Cell Endocrinol 321: 50–56. doi: 10.1016/j.mce.2009.10.013
[37]
Nikiforova MN, Lynch RA, Biddinger PW, Alexander EK, Dorn GW 2nd, et al. (2003) RAS point mutations and PAX8-PPAR gamma rearrangement in thyroid tumors: evidence for distinct molecular pathways in thyroid follicular carcinoma. J Clin Endocrinol Metab 88: 2318–2326. doi: 10.1210/jc.2002-021907
[38]
Copland JA, Marlow LA, Kurakata S, Fujiwara K, Wong AK, et al. (2006) Novel high-affinity PPARgamma agonist alone and in combination with paclitaxel inhibits human anaplastic thyroid carcinoma tumor growth via p21WAF1/CIP1. Oncogene 25: 2304–2317. doi: 10.1038/sj.onc.1209267
