http://iet.metastore.ingenta.com
1887

Down-regulation and clinical significance of miR-7-2-3p in papillary thyroid carcinoma with multiple detecting methods

Down-regulation and clinical significance of miR-7-2-3p in papillary thyroid carcinoma with multiple detecting methods

For access to this article, please select a purchase option:

Buy article PDF
$19.95
(plus tax if applicable)
Buy Knowledge Pack
10 articles for $120.00
(plus taxes if applicable)

IET members benefit from discounts to all IET publications and free access to E&T Magazine. If you are an IET member, log in to your account and the discounts will automatically be applied.

Learn more about IET membership 

Recommend Title Publication to library

You must fill out fields marked with: *

Librarian details
Name:*
Email:*
Your details
Name:*
Email:*
Department:*
Why are you recommending this title?
Select reason:
 
 
 
 
 
IET Systems Biology — Recommend this title to your library

Thank you

Your recommendation has been sent to your librarian.

Altered miRNA expression participates in the biological progress of thyroid carcinoma and functions as a diagnostic marker or therapeutic agent. However, the role of miR-7-2-3p is currently unclear. The authors’ study was the first investigation of miR-7-2-3p expression level and diagnostic ability in several public databases. Potential target genes were obtained from DIANA Tools, and function enrichment analysis was then performed. Furthermore, the authors examined expression levels of potential targets in the Human Protein Atlas (HPA) and the Cancer Genome Atlas (TCGA). Finally, the potential transcription factors (TFs) were predicted by JASPAR. TCGA, GSE62054, GSE73182, GSE40807, and GSE55780 revealed that miR-7-2-3p expression in papillary thyroid carcinoma (PTC) tissues was notably lower compared with non-tumour tissues, while its expression in E-MATB-736 showed no remarkable difference. Function enrichment analysis showed that 698 genes were enriched in pathways, including pathways in cancer, and glioma. CCND1, GSK3B, and ITGAV of pathways in cancer were inverse correlations with miR-7-2-3p in both post-transcription and protein levels. According to the TF prediction, the prospective upstream TFs of miR-7-2-3p were ISX, SPI1, PRRX1, and BARX1. MiR-7-2-3p was significantly down-regulated and may act on PTC progression by crucial pathways. However, the mechanisms of miR-7-2-3p need further investigation.

References

    1. 1)
      • 1. Siegel, R.L., Miller, K.D., Jemal, A.: ‘Cancer statistics, 2017’, CA Cancer J. Clin., 2017, 67, (1), pp. 730.
    2. 2)
      • 2. Davies, L., Welch, H.G.: ‘Current thyroid cancer trends in the United States’, JAMA Otolaryngol. Head Neck Surg., 2014, 140, (4), pp. 317322.
    3. 3)
      • 3. Pemayun, T.G.: ‘Current diagnosis and management of thyroid nodules’, Acta Med. Indones., 2016, 48, (3), pp. 247257.
    4. 4)
      • 4. Bartel, D.P.: ‘MicroRNAs: genomics, biogenesis, mechanism, and function’, Cell, 2004, 116, (2), pp. 281297.
    5. 5)
      • 5. Calin, G.A., Croce, C.M.: ‘MicroRNA signatures in human cancers’, Nat. Rev. Cancer, 2006, 6, (11), pp. 857866.
    6. 6)
      • 6. Chen, X., Xie, D., Zhao, Q., et al: ‘MicroRNAs and complex diseases: from experimental results to computational models’, Brief. Bioinf., 2019, 20, (2), pp. 515539.
    7. 7)
      • 7. Hwang, H.W., Mendell, J.T.: ‘MicroRNAs in cell proliferation, cell death, and tumorigenesis’, Br. J. Cancer, 2007, 96 Suppl, pp. R40R44.
    8. 8)
      • 8. Celano, M., Rosignolo, F., Maggisano, V., et al: ‘MicroRNAs as biomarkers in thyroid carcinoma’, Int. J. Genomics, 2017, 2017, (4), pp. 111.
    9. 9)
      • 9. Boufraqech, M., Klubo-Gwiezdzinska, J., Kebebew, E.: ‘MicroRNAs in the thyroid’, Best Pract. Res. Clin. Endocrinol. Metab., 2016, 30, (5), pp. 603619.
    10. 10)
      • 10. Kalinowski, F.C., Brown, R.A.M., Ganda, C., et al: ‘MicroRNA-7: a tumor suppressor miRNA with therapeutic potential’, Int. J. Biochem. Cell Biol., 2014, 54, pp. 312317.
    11. 11)
      • 11. Swierniak, M., Wojcicka, A., Czetwertynska, M., et al: ‘In-depth characterization of the microRNA transcriptome in normal thyroid and papillary thyroid carcinoma’, J. Clin. Endocrinol. Metab., 2013, 98, (8), pp. E1401E1409.
    12. 12)
      • 12. Saiselet, M., Gacquer, D., Spinette, A., et al: ‘New global analysis of the microRNA transcriptome of primary tumors and lymph node metastases of papillary thyroid cancer’, BMC Genomics, 2015, 16, p. 395.
    13. 13)
      • 13. Leek, J.T., Johnson, W.E., Parker, H.S., et al: ‘Sva: surrogate variable analysis’, R package version 3.30.1, 2019.
    14. 14)
      • 14. Vlachos, I.S., Zagganas, K., Paraskevopoulou, M.D., et al: ‘DIANA-miRPath V3.0: deciphering microRNA function with experimental support’, Nucleic Acids Res., 2015, 43, (W1), pp. W460W466.
    15. 15)
      • 15. Uhlen, M., Oksvold, P., Fagerberg, L., et al: ‘Towards a knowledge-based Human Protein Atlas’, Nat. Biotechnol., 2010, 28, (12), pp. 12481250.
    16. 16)
      • 16. Khan, A., Fornes, O., Stigliani, A., et al: ‘JASPAR 2018: update of the open-access database of transcription factor binding profiles and its web framework’, Nucleic Acids Res., 2018, 46, (D1), pp. D260D266.
    17. 17)
      • 17. Saiselet, M., Pita, J.M., Augenlicht, A., et al: ‘miRNA expression and function in thyroid carcinomas: a comparative and critical analysis and a model for other cancers’, Oncotarget, 2016, 7, (32), pp. 5247552492.
    18. 18)
      • 18. Chen, X., Xie, D., Wang, L., et al: ‘BNPMDA: bipartite network projection for miRNA–disease association prediction’, Bioinformatics, 2018, 34, (18), pp. 31783186.
    19. 19)
      • 19. Chen, X., Yin, J., Qu, J., et al: ‘MDHGI: matrix decomposition and heterogeneous graph inference for miRNA-disease association prediction’, PLoS Comput. Biol., 2018, 14, (8), p. e1006418.
    20. 20)
      • 20. Xie, M., Zhao, F., Zou, X., et al: ‘The association between CCND1 G870a polymorphism and colorectal cancer risk: a meta-analysis’, Medicine, 2017, 96, (42), p. e8269.
    21. 21)
      • 21. Liu, Y., Xu, X., Xu, X., et al: ‘Microrna-193a-3p inhibits cell proliferation in prostate cancer by targeting cyclin D1’, Oncol. Lett., 2017, 14, (5), pp. 51215128.
    22. 22)
      • 22. Bieche, I., Franc, B., Vidaud, D., et al: ‘Analyses of MYC, ERBB2, and CCND1 genes in benign and malignant thyroid follicular cell tumors by real-time polymerase chain reaction’, Thyroid, 2001, 11, (2), pp. 147152.
    23. 23)
      • 23. Ricarte-Filho, J.C., Fuziwara, C.S., Yamashita, A.S., et al: ‘Effects of let-7 microRNA on cell growth and differentiation of papillary thyroid cancer’, Transl. Oncol., 2009, 2, (4), pp. 236241.
    24. 24)
      • 24. Yin, Y., Hong, S., Yu, S., et al: ‘Mir-195 inhibits tumor growth and metastasis in papillary thyroid carcinoma cell lines by targeting CCND1 and FGF2’, Int. J. Endocrinol., 2017, 2017, p. 6180425.
    25. 25)
      • 25. McCubrey, J.A., Steelman, L.S., Bertrand, F.E., et al: ‘GSK-3 as potential target for therapeutic intervention in cancer’, Oncotarget, 2014, 5, (10), pp. 28812911.
    26. 26)
      • 26. Wang, J.-B., Wang, Z.-W., Li, Y., et al: ‘CDK5RAP3 acts as a tumor suppressor in gastric cancer through inhibition of beta-catenin signaling’, Cancer Lett., 2017, 385, pp. 188197.
    27. 27)
      • 27. Rath, G., Jawanjal, P., Salhan, S., et al: ‘Clinical significance of inactivated glycogen synthase kinase 3beta in HPV-associated cervical cancer: relationship with Wnt/beta-catenin pathway activation’, Am. J. Reprod. Immunol., 2015, 73, (5), pp. 460478.
    28. 28)
      • 28. Aristizabal-Pachon, A.F., Castillo, W.O.: ‘Role of GSK3beta in breast cancer susceptibility’, Cancer Biomark., 2017, 18, (2), pp. 169175.
    29. 29)
      • 29. Mishra, R., Nagini, S., Rana, A.: ‘Expression and inactivation of glycogen synthase kinase 3 alpha/beta and their association with the expression of cyclin D1 and P53 in oral squamous cell carcinoma progression’, Mol. Cancer, 2015, 14, (1), p. 20.
    30. 30)
      • 30. Shakoori, A., Ougolkov, A., Yu, Z.W., et al: ‘Deregulated GSK3beta activity in colorectal cancer: its association with tumor cell survival and proliferation’, Biochem. Biophys. Res. Commun., 2005, 334, (4), pp. 13651373.
    31. 31)
      • 31. Fu, Y., Wang, X., Cheng, X., et al: ‘Clinicopathological and biological significance of aberrant activation of glycogen synthase kinase-3 in ovarian cancer’, Onco. Targets Ther., 2014, 7, pp. 11591168.
    32. 32)
      • 32. Lu, J.G., Li, Y., Li, L., et al: ‘Overexpression of osteopontin and integrin αv in laryngeal and hypopharyngeal carcinomas associated with differentiation and metastasis’, J. Cancer Res. Clin. Oncol., 2011, 137, (11), pp. 16131618.
    33. 33)
      • 33. Hayashido, Y., Kitano, H., Sakaue, T., et al: ‘Overexpression of integrin alphav facilitates proliferation and invasion of oral squamous cell carcinoma cells via MEK/ERK signaling pathway that is activated by interaction of integrin alphavbeta8 with type collagen’, Int. J. Oncol., 2014, 45, (5), pp. 18751882.
    34. 34)
      • 34. Ding, Y., Pan, Y., Liu, S., et al: ‘Elevation of Mir-9-3p suppresses the epithelial-mesenchymal transition of nasopharyngeal carcinoma cells via down-regulating FN1, ITGB1 and ITGAV’, Cancer Biol. Ther., 2017, 18, (6), pp. 414424.
    35. 35)
      • 35. Flum, M., Kleemann, M., Schneider, H., et al: ‘miR-217-5p induces apoptosis by directly targeting PRKCI, BAG3, ITGAV and MAPK1 in colorectal cancer cells’, J. Cell. Commun. Signal., 2018, 12, (2), pp. 451466.
    36. 36)
      • 36. Mallik, S., Maulik, U.: ‘Mirna-Tf-gene network analysis through ranking of biomolecules for multi-informative uterine leiomyoma dataset’, J. Biomed. Inf., 2015, 57, pp. 308319.
    37. 37)
      • 37. Maulik, U., Sen, S., Mallik, S., et al: ‘Detecting TF-miRNA-gene network based modules for 5hmC and 5mC brain samples: a intra- and inter-species case-study between human and rhesus’, BMC Genet., 2018, 19, (1), p. 240.
    38. 38)
      • 38. Hsu, S.-H., Wang, L.-T., Lee, K.-T., et al: ‘Proinflammatory homeobox gene, ISX, regulates tumor growth and survival in hepatocellular carcinoma’, Cancer Res., 2013, 73, (2), pp. 508518.
    39. 39)
      • 39. Sue, S., Shibata, W., Kameta, E., et al: ‘Intestine-specific homeobox (ISX) induces intestinal metaplasia and cell proliferation to contribute to gastric carcinogenesis’, J. Gastroenterol., 2016, 51, (10), pp. 949960.
    40. 40)
      • 40. Seki, M., Kimura, S., Isobe, T., et al: ‘Recurrent Spi1 (Pu.1) fusions in high-risk pediatric T cell acute lymphoblastic leukemia’, Nat. Genet., 2017, 49, (8), pp. 12741281.
    41. 41)
      • 41. Ueno, N., Nishimura, N., Ueno, S., et al: ‘PU.1 acts as tumor suppressor for myeloma cells through direct transcriptional repression of IRF4’, Oncogene, 2017, 36, (31), pp. 44814497.
    42. 42)
      • 42. Goto, H., Kariya, R., Kudo, E., et al: ‘Restoring PU.1 induces apoptosis and modulates viral transactivation via interferon-stimulated genes in primary effusion lymphoma’, Oncogene, 2017, 36, (37), pp. 52525262.
    43. 43)
      • 43. Becker, J., May, A., Gerges, C., et al: ‘Supportive evidence for Foxp1, Barx1, and Foxf1 as genetic risk loci for the development of esophageal adenocarcinoma’, Cancer Med., 2015, 4, (11), pp. 17001704.
    44. 44)
      • 44. Wang, B., Chen, Q., Cao, Y., et al: ‘LGR5 is a gastric cancer stem cell marker associated with stemness and the EMT signature genes NANOG, NANOGP8, PRRX1, TWIST1, and BMI1’, PLoS ONE, 2016, 11, (12), p. e0168904.
    45. 45)
      • 45. Fan, M., Shen, J., Liu, H., et al: ‘Downregulation of PRRX1 via the p53-dependent signaling pathway predicts poor prognosis in hepatocellular carcinoma’, Oncol. Rep., 2017, 38, (2), pp. 10831090.
    46. 46)
      • 46. Hardin, H., Guo, Z., Shan, W., et al: ‘The roles of the epithelial-mesenchymal transition marker PRRX1 and miR-146b-5p in papillary thyroid carcinoma progression’, Am. J. Pathol., 2014, 184, (8), pp. 23422354.
http://iet.metastore.ingenta.com/content/journals/10.1049/iet-syb.2019.0025
Loading

Related content

content/journals/10.1049/iet-syb.2019.0025
pub_keyword,iet_inspecKeyword,pub_concept
6
6
Loading
This is a required field
Please enter a valid email address