open access

Vol 71, No 2 (2020)
Original paper
Submitted: 2019-11-06
Accepted: 2020-01-06
Published online: 2020-03-04
Get Citation

miR-1258: a novel microRNA that controls TMPRSS4 expression is associated with malignant progression of papillary thyroid carcinoma

Li-Juan Wang1, Han-Qing Cai1
·
Pubmed: 32154571
·
Endokrynol Pol 2020;71(2):146-152.
Affiliations
  1. Department of Endocrinology, The Second Hospital of Jilin University, Changchun, Jilin, China

open access

Vol 71, No 2 (2020)
Original Paper
Submitted: 2019-11-06
Accepted: 2020-01-06
Published online: 2020-03-04

Abstract

Background: MicroRNA-1258 (miR-1258) has been shown to play an anti-cancer role in a variety of cancers, but its relationship with papillary thyroid cancer (PTC) has not been reported. The emphasis of this research was to reveal the biological function of miR-1258 in PTC and its potential mechanisms. Material and methods: We measured miR-1258 expression in PTC cells and the transfection efficiency of miR-1258 mimic and miR-1258 inhibitor by quantitative real-time PCR (qRT-PCR) assay. Cell Counting Kit-8 assay (CCK8) and Transwell experiments were conducted to examine the influences of altering miR-1258 expression on the viability, migration, and invasion of PTC cells. Bioinformatics prediction and dual-luciferase experiment were performed to verify the target gene of miR-1258. Finally, we carried out a rescue assay to verify whether the regulation of miR-1258 on the biological behaviour of PTC cells needs to be achieved by regulating TMPRSS4. Results: The outcomes revealed that miR-1258 was lowly expressed in PTC cell lines and miR-1258 showed the lowest expression in KTC-1 and the highest expression in B-CPAP among all tested PTC cell lines. Overexpression of miR-1258 inhibited KTC-1 cell viability and ability to migrate and invade, whereas inhibition of miR-1258 in B-CPAP cells has the opposite effect. Furthermore, we affirmed that miR-1258 can directly target TMPRSS4, and miR-1258 can reduce the biological malignant behaviour of PTC cells via regulation of TMPRSS4. Conclusion: Taken together, our research raised the possibility that miR-1258 was an anti-oncogene, which exerts its anti-cancer function by targeting TMPRSS4. Hence, it may be possible to treat PTC by targeting the miR-1258/TMPRSS4 axis in the future. 

Abstract

Background: MicroRNA-1258 (miR-1258) has been shown to play an anti-cancer role in a variety of cancers, but its relationship with papillary thyroid cancer (PTC) has not been reported. The emphasis of this research was to reveal the biological function of miR-1258 in PTC and its potential mechanisms. Material and methods: We measured miR-1258 expression in PTC cells and the transfection efficiency of miR-1258 mimic and miR-1258 inhibitor by quantitative real-time PCR (qRT-PCR) assay. Cell Counting Kit-8 assay (CCK8) and Transwell experiments were conducted to examine the influences of altering miR-1258 expression on the viability, migration, and invasion of PTC cells. Bioinformatics prediction and dual-luciferase experiment were performed to verify the target gene of miR-1258. Finally, we carried out a rescue assay to verify whether the regulation of miR-1258 on the biological behaviour of PTC cells needs to be achieved by regulating TMPRSS4. Results: The outcomes revealed that miR-1258 was lowly expressed in PTC cell lines and miR-1258 showed the lowest expression in KTC-1 and the highest expression in B-CPAP among all tested PTC cell lines. Overexpression of miR-1258 inhibited KTC-1 cell viability and ability to migrate and invade, whereas inhibition of miR-1258 in B-CPAP cells has the opposite effect. Furthermore, we affirmed that miR-1258 can directly target TMPRSS4, and miR-1258 can reduce the biological malignant behaviour of PTC cells via regulation of TMPRSS4. Conclusion: Taken together, our research raised the possibility that miR-1258 was an anti-oncogene, which exerts its anti-cancer function by targeting TMPRSS4. Hence, it may be possible to treat PTC by targeting the miR-1258/TMPRSS4 axis in the future. 

Get Citation

Keywords

miR-1258; TMPRSS4; target; PTC

About this article
Title

miR-1258: a novel microRNA that controls TMPRSS4 expression is associated with malignant progression of papillary thyroid carcinoma

Journal

Endokrynologia Polska

Issue

Vol 71, No 2 (2020)

Article type

Original paper

Pages

146-152

Published online

2020-03-04

Page views

1648

Article views/downloads

836

DOI

10.5603/EP.a2020.0009

Pubmed

32154571

Bibliographic record

Endokrynol Pol 2020;71(2):146-152.

Keywords

miR-1258
TMPRSS4
target
PTC

Authors

Li-Juan Wang
Han-Qing Cai

References (30)
  1. Miccoli P, Bakkar S. Surgical management of papillary thyroid carcinoma: an overview. Updates Surg. 2017; 69(2): 145–150.
  2. Pusztaszeri M, Auger M. Update on the cytologic features of papillary thyroid carcinoma variants. Diagn Cytopathol. 2017; 45(8): 714–730.
  3. Wang Y, Han J, Lv Y, et al. miR-29a inhibits proliferation, invasion, and migration of papillary thyroid cancer by targeting DPP4. Onco Targets Ther. 2019; Volume 12: 4225–4233.
  4. Fagin JA, Wells SA. Biologic and Clinical Perspectives on Thyroid Cancer. N Engl J Med. 2016; 375(23): 2307.
  5. Xing M, Alzahrani AS, Carson KA, et al. Association between BRAF V600E mutation and recurrence of papillary thyroid cancer. J Clin Oncol. 2015 ; 1(33): 42–50.
  6. Zang C, Sun J, Liu W, et al. miRNA-21 promotes cell proliferation and invasion via VHL/PI3K/AKT in papillary thyroid carcinoma. Hum Cell. 2019; 32(4): 428–436.
  7. Kilfoy BA, Devesa SS, Ward MH, et al. Gender is an Age-Specific Effect Modifier for Papillary Cancers of the Thyroid Gland. Cancer Epidemiol Biomarkers Prev. 2009; 18(4): 1092–1100.
  8. Zhang W, Sun W, Qin Y, et al. Knockdown of KDM1A suppresses tumour migration and invasion by epigenetically regulating the TIMP1/MMP9 pathway in papillary thyroid cancer. J Cell Mol Med. 2019; 23(8): 4933–4944.
  9. Rupaimoole R, Slack FJ. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases. Nat Rev Drug Discov. 2017; 16(3): 203–222.
  10. Setoyama T, Ling H, Natsugoe S, et al. Non-coding RNAs for medical practice in oncology. Keio J Med. 2011; 60(4): 106–113.
  11. Chan B, Manley J, Lee J, et al. The emerging roles of microRNAs in cancer metabolism. Cancer Lett. 2015; 356(2 Pt A): 301–8.
  12. Xiang D, Tian B, Yang T, et al. miR-222 expression is correlated with the ATA risk stratifications in papillary thyroid carcinomas. Medicine (Baltimore). 2019; 98(25): e16050.
  13. Yin JJ, Cheng XY. MicroRNA-23a inhibits the growth of papillary thyroid carcinoma via regulating cyclin G1. Eur Rev Med Pharmacol Sci. 2019; 23(8): 3431–3439.
  14. Liu ZM, Wu ZY, Li WH, et al. MiR-96-5p promotes the proliferation, invasion and metastasis of papillary thyroid carcinoma through down-regulating CCDC67. Eur Rev Med Pharmacol Sci. 2019; 23(8): 3421–3430.
  15. Zhu J, Zhang Q, Jin XY, et al. MiR-506 suppresses papillary thyroid carcinoma cell proliferation and metastasis via targeting IL17RD. Eur Rev Med Pharmacol Sci. 2019; 23(7): 2856–2862.
  16. Liu F, Yin R, Chen X, et al. Over-expression of miR-206 decreases the Euthyrox-resistance by targeting MAP4K3 in papillary thyroid carcinoma. Biomed Pharmacother. 2019; 114: 108605.
  17. Jiang W, Wei Ke, Pan C, et al. MicroRNA-1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non-small-cell lung cancer. Cell Prolif. 2018; 51(6): e12502.
  18. Filippova EA, Loginov VI, Burdennyi AM, et al. Hypermethylated Genes of MicroRNA in Ovarian Carcinoma: Metastasis Prediction Marker Systems. Bull Exp Biol Med. 2019; 167(1): 79–83.
  19. Liu W, Zhou Z, Zhang Qi, et al. Overexpression of miR-1258 inhibits cell proliferation by targeting AKT3 in osteosarcoma. Biochem Biophys Res Commun. 2019; 510(3): 479–486.
  20. Zhang H, Jiang S, Guo L, et al. MicroRNA-1258, regulated by c-Myb, inhibits growth and epithelial-to-mesenchymal transition phenotype via targeting SP1 in oral squamous cell carcinoma. J Cell Mol Med. 2019; 23(4): 2813–2821.
  21. Zhang Z, Li J, Huang Y, et al. Upregulated miR-1258 regulates cell cycle and inhibits cell proliferation by directly targeting E2F8 in CRC. Cell Prolif. 2018; 51(6): e12505.
  22. Shi J, Chen P, Sun J, et al. MicroRNA-1258: An invasion and metastasis regulator that targets heparanase in gastric cancer. Oncol Lett. 2017; 13(5): 3739–3745.
  23. Hu M, Wang M, Lu H, et al. Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B. Oncotarget. 2016; 7(28): 43419–43431.
  24. Zou H, Xu X, Luo L, et al. Hsa_circ_0101432 promotes the development of hepatocellular carcinoma (HCC) by adsorbing miR-1258 and miR-622. Cell Cycle. 2019; 18(19): 2398–2413.
  25. Tanabe LM, List K. The role of type II transmembrane serine protease-mediated signaling in cancer. FEBS J. 2017; 284(10): 1421–1436.
  26. Cheng Y, Wang K, Geng L, et al. Identification of candidate diagnostic and prognostic biomarkers for pancreatic carcinoma. EBioMedicine. 2019; 40: 382–393.
  27. Yuan H, Chen Z, Bai S, et al. Molecular mechanisms of lncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis in gastric cancer. Cancer Lett. 2018; 418: 84–96.
  28. Fan X, Liang Y, Liu Y, et al. The upregulation of TMPRSS4, partly ascribed to the downregulation of miR‑125a‑5p, promotes the growth of human lung adenocarcinoma via the NF‑κB signaling pathway. Int J Oncol. 2018; 53(1): 148–158.
  29. Mahati S, Bolati D, Yang Y, et al. TMPRSS4 promotes cancer stem cell traits by regulating CLDN1 in hepatocellular carcinoma. Biochem Biophys Res Commun. 2017; 490(3): 906–912.
  30. Li XM, Liu WL, Chen Xu, et al. Overexpression of TMPRSS4 promotes tumor proliferation and aggressiveness in breast cancer. Int J Mol Med. 2017; 39(4): 927–935.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą jest  VM Media Group sp. z o.o., Grupa Via Medica, ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl