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. 2020 Jan 30;20:34. doi: 10.1186/s12935-020-1105-6

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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. 4 — YTHDF2 is crucial for ALKBH5-mediated suppression of PVT1 degradation. a The RIP assays using YTHDF2, YTHDF3 and YTHDC2 antibodies were carried out in MG63 and H2OS cells. b The effect of ALKBH5 knockdown on the interaction between YTHDF2 and PVT1 was measured using anti-YTHDF2 RIP assay in MG63 and H2OS cells. c The effect of ALKBH5 overexpression on the interaction between YTHDF2 and PVT1 was measured using anti-YTHDF2 RIP assay in 143B cells. d The YTHDF2 expression was knocked down in ALKBH5-overexpressed 143B cells. e The PVT1 level in ALKBH5-overexpressed 143B cells transfected with YTHDF2 shRNA. f The stability of PVT1 over time in ALKBH5-overexpressed 143B cells transfected with YTHDF2 shRNA was measured by qRT-PCR relative to time 0. *p < 0.05, ***p < 0.001