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. 2021 Nov 8;33(Suppl 1):e922–e932. doi: 10.1097/MEG.0000000000002309

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Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Fig. 6. — KIF9-AS1 promoted the dextran sulfate sodium (DSS)-induced apoptosis of colonic cells by targeting miR-148a-3p/suppressor of cytokine signaling (SOCS3) axis. (a) The protein expression of SOCS3 was markedly enhanced in DSS-induced HT-29 cells. ^**P < 0.01 vs. control; (b) the transfection efficiency of pcDNA-NC and pcDNA-SOCS3 was demonstrated using quantitative real time PCR (qRT-PCR) in DSS-induced HT-29 cells. ^**P < 0.01 vs. pcDNA-NC; (c and d) Inhibition of miR-148a-3p or overexpression of SOCS3 weakened the inhibitory effect of KIF9-AS1 silencing on the apoptosis rate and caspase-3 protein expression of DSS-induced HT-29 cells. ^**P < 0.01 vs. si-NC; ^##P < 0.01 vs. si-KIF9-AS1.