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. 2020 Jan-Dec:29:963689720918300.
doi: 10.1177/0963689720918300.

Validation of MicroRNA-188-5p Inhibition Power on Tumor Cell Proliferation in Papillary Thyroid Carcinoma

Ping Zhou  1 , Andrew Irving  2 , Huifang Wu  3 , Juan Luo  3 , Johana Aguirre  4 , Mariana Costa  4 , Monny Khamsuree  5 , Natascha Gerads  5 , Weibang Liu  3
Affiliations

Validation of MicroRNA-188-5p Inhibition Power on Tumor Cell Proliferation in Papillary Thyroid Carcinoma

Ping Zhou et al. Cell Transplant. 2020 Jan-Dec.

Abstract

Given the crucial role of microRNAs in the cellular proliferation of various types of cancers, we aimed to analyze the expression and function of a cellular proliferation-associated miR-188-5p in papillary thyroid carcinoma (PTC). Here we demonstrate that miR-188-5p is downregulated in PTC tumor tissues compared with the associated noncancerous tissues. We also validate that the miR-188-5p overexpression suppressed the PTC cancer cell proliferation. In addition, fibroblast growth factor 5 (FGF5) is observed to be downregulated in the PTC tumor tissues compared with the associated noncancerous tissues. Subsequently, FGF5 is identified as the direct functional target of miR-188-5p. Moreover, the silencing of FGF5 was found to inhibit PTC cell proliferation, which is the same pattern as miR-188-5p overexpression. These results suggest that miR-188-5p-associated silencing of FGF5 inhibits tumor cell proliferation in PTC. It also highlights the importance of further evaluating miR-188-5p as a potential biomarker and therapy target in PTC.

Keywords: FGF5; cell proliferation; miR-188-5p.

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Conflict of interest statement

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Fig. 1.
Fig. 1.
miR-188-5p expression was downregulated in PTC tissues. (A) miR-188-5p expression was determined by qualitative real-time polymerase chain reaction in 12 paired PTC and adjacent nontumor tissues. *P < 0.05 vs. nontumor tissues (n = 12); (B) miR-188-5p expression in TPC-1, K1, and Nithy. Results are mean ± standard error (n = 3). *P < 0.05 vs. Nithy-ori 3-1. miR: microRNA; PTC: papillary thyroid carcinoma.
Fig. 2.
Fig. 2.
Effect of miR-188-5p on PTC cell proliferation. (A) PTC cells were infected with miR-188-5p lentivirus or miR-NC. miR-188-5p was determined by qualitative real-time polymerase chain reaction; (B) TPC-1/K1 cells or TPC-1/K1 infected with miR-188-5p or miR-NC cells were seeded into 96-well plates. Cyquant assay was performed to determine the cell proliferation. Results are mean ± standard error (n = 3). *P < 0.05 vs. WT; **P < 0.05 vs. miR-NC. miR: microRNA; PTC: papillary thyroid carcinoma; WT: wild type
Fig. 3.
Fig. 3.
Soft agar assay was performed to determine the anchorage-independent growth of TPC-1 and K1 cells after miR-188-5p overexpression.
Fig. 4.
Fig. 4.
FGF5 expression was upregulated in PTC tissues. (A) FGF5 mRNA level was determined by qualitative real-time polymerase chain reaction in 12 paired PTC and adjacent nontumor tissues. *P < 0.05 vs. nontumor tissues (n = 12); (B) FGF5 protein expression level was determined by western blotting in 12 paired PTC and adjacent nontumor tissues. FGF5: fibroblast growth factor 5; PTC: papillary thyroid carcinoma.
Fig. 5.
Fig. 5.
FGF5 is the direct target gene of miR-188-5p. (A) Confirm FGF5 is the direct target gene of miR-188-5p by dual-luciferase assay; (B) FGF5 mRNA level was significantly decreased after miR-188-5p overexpression, which was detected by qualitative real-time polymerase chain reaction; (C) FGF5 protein expression was remarkably decreased after miR-188-5p overexpression, as determined by western blotting. Results are mean ± standard error (n = 3). *P < 0.05 vs. WT; **P < 0.05 vs. miR-NC. FGF5: fibroblast growth factor 5; miR: microRNA; WT: wild type.
Fig. 6.
Fig. 6.
Effect of FGF5 silencing on PTC cell proliferation. (A) PTC cells were infected with sh-FGF5 lentivirus or sh-Ctrl. FGF5 protein expression was determined by western blotting; (B) TPC-1/K1 cells or TPC-1/K1 infected with sh-Ctrl or sh-FGF5 cells were seeded into 96-well plates. Cyquant assay was performed to determine the cell proliferation. Results are mean ± standard error (n = 3). *P < 0.05 vs. WT; **P < 0.05 vs. sh-FGF5. Soft agar assay was performed to determine the anchorage-independent growth of TPC-1 and K1 cells after FGF5 silencing. FGF5: fibroblast growth factor 5; PTC: papillary thyroid carcinoma; WT: wild type.
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References

    1. Brito JP, Kim HJ, Han SJ, Lee YS, Ahn HS. Geographic distribution and evolution of thyroid cancer epidemic in South Korea. Thyroid. 2016;26(6):864–865. - PubMed
    1. Chen W, Zheng R, Baade PD, Zhang S, Zeng H, Bray F, Jemal A, Yu XQ, He J. Cancer statistics in China, 2015. CA Cancer J Clin. 2016;66(2):115–132. - PubMed
    1. Guo H, Ingolia NT, Weissman JS, Bartel DP. Mammalian microRNAs predominantly act to decrease target mRNA levels. Nature. 2010;466(7308):835–840. - PMC - PubMed
    1. Kohlhapp FJ, Mitra AK, Lengyel E, Peter ME. MicroRNAs as mediators and communicators between cancer cells and the tumor microenvironment. Oncogene. 2015;34(48):5857–5868. - PMC - PubMed
    1. Lee RC, Feinbaum RL, Ambros V. The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14. Cell. 1993;75(5):843–854. - PubMed