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. 2021 Mar 4;12(1):763–778. doi: 10.1080/21655979.2021.1880717

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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Overexpression of miR-574-3p diminished the antitumor effects of NK cells and IL-18

a. qPCR was used to assess expression of miR-574-3p. Increased expression of miR-574-3p after transient transfection of miR-574-3p mimics. b. MTS assay showing that miR-574-3p mimics partially restored the cells proliferation rate of HCT116 with NK cells coculturing and IL-18 treatment. c. Representative fluorescence-activated cells sorting of 7-AAD positive and annexin V-positive cells of HCT116 when miR-574-3p was expressed. The overexpression of miR-574-3p alone did not change the apoptotic rate of HCT116 but rescued the HCT116 from apoptosis with NK cells coculturing and IL-18 treatment. d. qPCR results indicated that overexpression of miR-574-3p significantly reduced the expression of TGF-β1. NK: Natural killer; IL-18: Interleukin 18; MTS: 3-(4,5-Dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium; qPCR: Quantitative polymerase chain reaction; TGF-β1: Transforming growth factor beta 1, con: control grouop; NC: negative control of miR-574-3p mimics group. All data with error bars are presented as mean + SD, One-way analysis: * p < 0.05, compared with Con groupns; # p < 0.05, compared with NC groupns; ns: not significant.