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. 2022 Feb 25;163(4):bqac022. doi: 10.1210/endocr/bqac022

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© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 5. — Induction of miR-205-5p attenuates GGCT-mediated PTC cell proliferation, migration, invasion, EMT process, tumorigenic ability, and distant metastatic potential to the lung. (a) Cell viability was examined by CCK8 after overexpression of miR-205-5p in K1-Control or K1-GGCT cell lines. Cell migration (b-c) and invasion (d-e) potentials were determined by wound healing and transwell assays. (f) Expression of epithelial marker (E-cadherin) and mesenchymal markers (N-cadherin, CD44, MMP2 and MMP9) was analyzed by Western blotting after miR-205-5p overexpression in K1-GGCT cells. (g) Quantification of WB experiments was normalized to β-Actin control. (h) Tumorigenic ability was assessed after miR-205-5p overexpression in K1-GGCT cells. (i) Dissected tumor weights in each group were depicted as dot plots. (j) Tumor lung metastasis was assayed after miR-205-5p overexpression in K1-GGCT cells. (k) The histogram denotes luciferase bioluminescence emitted from the lungs in each group 21 days post tumor injection. **: P < 0.01, ***: P < 0.001.