Triiodothyronine Promotes Cell Proliferation of Breast Cancer via Modulating miR-204/Amphiregulin
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Breast cancer (BC) severely threatens women’s life, and Triiodothyronine (T3) shows a positive role on BC cell proliferation, while the potential mechanism underlying it is still unclear. T3 was used to stimulate BC cell lines MCF-7 and T47-D. Real-time PCR was performed to determine the expression of miRNAs, while western blot was used to measure protein expression of Amphiregulin (AREG), AKT and p-AKT. The interaction between miR-204 and AREG was determined using luciferase reporter assay. MTT was performed to detect cell viability. The expression of miR-204 was decreased, while AREG and p-AKT was increased in T3 stimulated BC cell lines. T3 stimulation promoted cell viability. miR-204 targets AREG to regulate its expression. T3 promoted expression of AREG and p-AKT, while miR-204 overexpression reversed the effect of T3, however, pcDNA-AREG transfection abolished the effect of miR-204 mimic. T3 promoted cell viability of BC cells via modulating the AKT signaling pathway. The detailed mechanism was that the down-regulated miR-204 that induced by T3 stimulation promoted the expression of AREG, the up-regulated AREG activated AKT signaling pathway, while the activated AKT signaling promoted cell proliferation.
KeywordsBreast cancer T3 Cell viability miR-204 AREG
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no conflict of interest.
Research Involving Human Participants and/or Animals
This article does not contain any studies with human participants or animals performed by any of the authors.
- 16.Li W, Jin X, Zhang Q, Zhang G, Deng X, Ma L (2014) Decreased expression of miR-204 is associated with poor prognosis in patients with breast cancer. Int J Clin Exp Pathol 7:3287–3292Google Scholar
- 19.Figueiredo NB, Cestari SH, Conde SJ, Luvizotto RA, De Sibio MT, Perone D, Katayama ML, Carraro DM, Brentani HP, Brentani MM, Nogueira CR (2014) Estrogen-responsive genes overlap with triiodothyronine-responsive genes in a breast carcinoma cell line. ScientificWorldJournal 2014:969404Google Scholar
- 22.Sacconi A, Biagioni F, Canu V, Mori F, Di Benedetto A, Lorenzon L, Ercolani C, Di Agostino S, Cambria AM, Germoni S, Grasso G, Blandino R, Panebianco V, Ziparo V, Federici O, Muti P, Strano S, Carboni F, Mottolese M, Diodoro M, Pescarmona E, Garofalo A, Blandino G (2012) miR-204 targets Bcl-2 expression and enhances responsiveness of gastric cancer. Cell Death Dis 3:e423CrossRefGoogle Scholar
- 26.Wu L, Chen Z, Xing Y (2018) MiR-506-3p inhibits cell proliferation, induces cell cycle arrest and apoptosis in retinoblastoma by directly targeting NEK6. Cell Biol Int. https://doi.org/10.1002/cbin.11041
- 27.Zhou S, Li S, Zhang W, Tong H, Li S, Yan Y (2018) MiR-139 promotes differentiation of bovine skeletal muscle-derived satellite cells by regulating DHFR gene expression. J Cell Physiol 234(1):632–641Google Scholar
- 30.Li X, Liu H, Wang J, Qin J, Bai Z, Chi B, Yan W, Chen X (2018) Curcumol induces cell cycle arrest and apoptosis by inhibiting IGF-1R/PI3K/Akt signaling pathway in human nasopharyngeal carcinoma CNE-2 cells. Phytother Res 32(11):2214–2225Google Scholar
- 31.Kim JW, Kim DK, Min A, Lee KH, Nam HJ, Kim JH, Kim JS, Kim TY, Im SA, Park IA (2016) Amphiregulin confers trastuzumab resistance via AKT and ERK activation in HER2-positive breast cancer. J Cancer Res Clin Oncol 142(1):157–165Google Scholar