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. 2020 Jul 24;20:340. doi: 10.1186/s12935-020-01425-2

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — KCNQ1OT1knockdown suppressed CRC tumor growth by regulating of miR-329-3p/CTNND1axis in vivo. a, b Tumor volume and tumor weight were measured in xenografts. c The expression levels of KCNQ1OT1,miR-329-3p and CTNND1 in xenografts were assessed by RT-qPCR. d CTNND1 protein level was detected in xenografts. The protein levels of CyclinD1, Bcl-2, and Cleaved-casp-3 were measured in xenografts. e The expression levels of CyclinD1, apoptosis-associated proteins (Bcl-2, Cleaved-casp-3) and the control (GAPDH) were evaluated by western blot in xenografts transfected with sh-KCNQ1OT1 or sh-control. *P < 0.05, vs. control group