Hsa_circ_0002111/miR-557/DUSP14 axis mediates euthyrox-resistance in papillary thyroid cancer
Abstract
As one of the most commonly used chemotherapeutic drug for papillary thyroid cancer (PTC), euthyrox affects the therapeutic outcome due to the resistance of euthyrox. Hsa_circ_0002111 is highly expressed in euthyrox-resistant PTC patients, and this study intends to explore its role in euthyrox drug resistance. PTC patient samples were used to screen for Circ_0002111 expression. TPC-1 and K1 PTC cell lines and their corresponding euthyrox-resistant cell lines (TPC-1/euthyrox and K1/euthyrox), and a benign human thyroid follicular cell line (Nthy-ori 3-1) were used in in vitro experiments. Circ_0002111 was knocked down in euthyrox-resistant cell lines, and cell viability and colony formation were detected. Caspase-3 activity assay and nucleosomal fragmentation assay were used for the detection of apoptosis. Luciferase reporter assay and biotin-labeled RNA pulldown assay were used to analyze interactions between Circ_0002111 and miR-557, or miR-557 and DUSP14. The upregulation of Circ_0002111 was found in PTC patient samples and associated with euthyrox-resistance in poor prognosis of PTC patients. Experiments in cell lines showed that Circ_0002111 regulates euthyrox-resistance in PTC cells. Mechanistic studies showed that Circ_0002111 promoted DUSP14 expression through miR-557, and euthyrox-resistance in PTC cells depended on the regulation via miR-557/DUSP14 signaling pathways. In conclusion, Hsa_circ_0002111 promotes euthyrox-resistance of PTC cells by adsorption miR-557 upregulation, suggesting Circ_0002111 might be a potential diagnostic marker and therapeutic target for euthyrox-resistant PTC patients.
Downloads
References
Cabanillas ME, McFadden DG, Durante C. Thyroid cancer. Lancet 2016; 388: 2783–95. doi: 10.1016/S0140-6736(16)30172-6
Wiltshire JJ, Drake TM, Uttley L, Balasubramanian SP. Systematic review of trends in the incidence rates of thyroid cancer. Thyroid 2016; 26: 1541–52. doi: 10.1089/thy.2016.0100
Mao YS, Xing MZ. Recent incidences and differential trends of thyroid cancer in the USA. Endocr Relat Cancer 2016; 23: 313–22. doi: 10.1530/ERC-15-0445
Aragon Han P, Weng CH, Khawaja HT, Nagarajan N, Schneider EB, Umbricht CB, et al. MicroRNA expression and association with clinicopathologic features in papillary thyroid cancer: a systematic review. Thyroid 2015; 25: 1322–9. doi: 10.1089/thy.2015.0193
Kunavisarut T. Diagnostic biomarkers of differentiated thyroid cancer. Endocrine 2013; 44: 616–22. doi: 10.1007/s12020-013-9974-2
Lundgren CI, Hall P, Dickman PW, Zedenius J. Clinically significant prognostic factors for differentiated thyroid carcinoma: a population-based, nested case-control study. Cancer 2006; 106: 524–31. doi: 10.1002/cncr.21653
Fiore E, Rago T, Latrofa F, Provenzale MA, Piaggi P, Delitala A, et al. Hashimoto’s thyroiditis is associated with papillary thyroid carcinoma: role of TSH and of treatment with L-thyroxine. Endocr Relat Cancer 2011; 18: 429–37. doi: 10.1530/ERC-11-0028
Han B, Chao J, Yao HH. Circular RNA and its mechanisms in disease: from the bench to the clinic. Pharmacol Ther 2018; 187: 31–44. doi: 10.1016/j.pharmthera.2018.01.010
Nicolet BP, Engels S, Aglialoro F, van den Akker E, von Lindern M, Wolkers MC. Circular RNA expression in human hematopoietic cells is widespread and cell-type specific. Nucleic Acids Res 2018; 46: 8168–80. doi: 10.1093/nar/gky721
Salzman J. Circular RNA Expression: its potential regulation and function. Trends Genet 2016; 32: 309–16. doi: 10.1016/j.tig.2016.03.002
Jin XY, Wang ZY, Pang WY, Zhou J, Liang Y, Yang JJ, et al. Upregulated hsa_circ_0004458 contributes to progression of papillary thyroid carcinoma by inhibition of miR-885-5p and activation of RAC1. Med Sci Monit 2018; 24: 5488–500. doi: 10.12659/MSM.911095
Tian XF, Zhang L, Jiao Y, Chen JS, Shan Y, Yang WF. CircABCB10 promotes nonsmall cell lung cancer cell proliferation and migration by regulating the miR-1252/FOXR2 axis. J Cell Biochem 2019; 120: 3765–72. doi: 10.1002/jcb.27657
Yao Y, Chen XY, Yang H, Chen W, Qian YC, Yan ZY, et al. Hsa_circ_0058124 promotes papillary thyroid cancer tumorigenesis and invasiveness through the NOTCH3/GATAD2A axis. J Exp Clin Cancer Res 2019; 38: 318. doi: 10.1186/s13046-019-1321-x
Li QD, Wang YC, Wu S, Zhou Z, Ding XJ, Shi RH, et al. CircACC1 regulates assembly and activation of AMPK complex under metabolic stress. Cell Metab 2019; 30: 157–73.e7. doi: 10.1016/j.cmet.2019.05.009
Zhao HD, Tang HL, Huang QK, Qiu B, Liu XM, Fan D, et al. MiR-101 targets USP22 to inhibit the tumorigenesis of papillary thyroid carcinoma. Am J Cancer Res 2016; 6: 2575–86.
Wang Z. Editorial (hot topic: miRNAs as legitimate targets for cancer therapy). Curr Drug Targets 2013; 14: 1093. doi: 10.2174/1389450111314100001
Shao H, Zhang Y, Yan J, Ban X, Fan X, Chang X, et al. Upregulated MicroRNA-483-3p is an early event in pancreatic ductal adenocarcinoma (PDAC) and as a powerful liquid biopsy biomarker in PDAC. Onco Targets Ther 2021; 14: 2163–75. doi: 10.2147/OTT.S288936
Panda AC. Circular RNAs act as miRNA sponges. Adv Exp Med Biol 2018; 1087: 67–79. doi: 10.1007/978-981-13-1426-1_6
Qiu J, Hao Y, Huang S, Ma Y, Li X, Li D, et al. MiR-557 works as a tumor suppressor in human lung cancers by negatively regulating LEF1 expression. Tumour Biol 2017; 39: 1010428317709467. doi: 10.1177/1010428317709467
Yang Y, Sun KK, Shen XJ, Wu XY, Li DC. miR-557 inhibits the proliferation and invasion of pancreatic cancer cells by targeting EGFR. Int J Clin Exp Pathol 2019; 12: 1333–41.
Kia V, Paryan M, Mortazavi Y, Biglari A, Mohammadi-Yeganeh S. Evaluation of exosomal miR-9 and miR-155 targeting PTEN and DUSP14 in highly metastatic breast cancer and their effect on low metastatic cells. J Cell Biochem 2019; 120: 5666–76. doi: 10.1002/jcb.27850
Mabrouk NMK, Elkaffash DM, Abdel-Hadi M, Abdelmoneim SE, Saad ElDeen S, Gewaifel G, et al. Identification of the possible therapeutic targets in the insulin-like growth factor 1 receptor pathway in a cohort of Egyptian hepatocellular carcinoma complicating chronic hepatitis C type 4. Drug Target Insights 2020; 14: 1–11. doi: 10.33393/dti.2020.1548
Wei Y, Wang G, Wang C, Zhou Y, Zhang J, Xu K. Upregulation of DUSP14 affects proliferation, invasion and metastasis, potentially via epithelial-mesenchymal transition and is associated with poor prognosis in pancreatic cancer. Cancer Manag Res 2020; 12: 2097–108. doi: 10.2147/CMAR.S240040
Yan F, Ying L, Li X, Qiao B, Meng Q, Yu L, et al. Overexpression of the transcription factor ATF3 with a regulatory molecular signature associates with the pathogenic development of colorectal cancer. Oncotarget 2017; 8: 47020–36. doi: 10.18632/oncotarget.16638
Ashraf S, Hegazy YK, Harmancey R. Nuclear receptor subfamily 4 group A member 2 inhibits activation of ERK signaling and cell growth in response to beta-adrenergic stimulation in adult rat cardiomyocytes. Am J Physiol Cell Physiol 2019; 317: C513–24. doi: 10.1152/ajpcell.00526.2018
Douglas T, Saleh M. Post-translational modification of OTULIN regulates ubiquitin dynamics and cell death. Cell Rep 2019; 29: 3652–63.e5. doi: 10.1016/j.celrep.2019.11.014
Jianrong S, Yanjun Z, Chen Y, Jianwen X. DUSP14 rescues cerebral ischemia/reperfusion (IR) injury by reducing inflammation and apoptosis via the activation of Nrf-2. Biochem Biophys Res Commun 2019; 509: 713–21. doi: 10.1016/j.bbrc.2018.12.170
Copyright (c) 2022 Jing Zhou, Jing Liu, Weiyuan Ma, Pengxin Zhao
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors retain full copyright to their individual works, and publishing rights without restrictions.
In accordance with the Budapest Open Access Initiative, articles published in STEMedicine are freely available "on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited."
Except where otherwise noted, all content on this website is licensed under a Creative Commons Attribution 4.0 License. This license allows for commercial and non-commercial redistribution as well as modifications of the work as long as attribution is given to the authors and STEMedicine as the original publication source, and a link to the article on the STEMedicine website is provided.
