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. 2020 Jul 24;20:338. doi: 10.1186/s12935-020-01419-0

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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. 6 — Effect of HOTAIR on sunitinib resistance of nude mouse xenografts. The nude mice were injected with 786-O-R or ACHN-R cells to establish xenograft models, followed by sunitinib treatment and sh-HOTAIR (sh-NC) injection. Tumor size was weekly recorded. Injection with sh-HOTAIR amplified the inhibitory effect of sunitinib on RC (a). qRT-PCR, Western blot, and immunohistochemistry were adopted to assay the expressions of HOTAIR (b), miR-17-5p (c), Beclin1 (d, e), LC3-II/LC3-I (f), p62 (f), and Ki67 (g). Injection with sh-HOTAIR heightened levels of miR-17-5p and p62, restrained HOTAIR expression, as well as decreased Beclin1 and LC3-II/LC3-I. Additionally, knockdown of HOTAIR in RC nude mice inhibited proliferation of tumor; ^*P < 0.05, ^**P < 0.01, compared to suni + sh-NC group or 786-O-R + suni + sh-NC or ACHN-R + suni + sh-NC; RC, renal cancer