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. 2021 Aug 27;40:272. doi: 10.1186/s13046-021-02074-7

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© The Author(s) 2021

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 — Circ-GALNT16 is mainly localized in the nucleus and binds to the KH3 domain of hnRNPK. a, b. Subcellular fractionation and FISH assays indicated that circ-GALNT16 was predominately localized in the nucleus of CRC cells. c-e. RNA pulldown assay followed by silver staining, MS, and RIP assay indicated that circ-GALNT16 specifically interacted with hnRNPK. f. Dual RNA FISH and immunofluorescence assays showed that circ-GALNT16 and hnRNPK colocalized in the nucleus of DLD-1 and LoVo. g. Functional domain and truncated mutation annotation of hnRNPK. h-i. RIP assay and RNA pulldown assay confirmed that circ-GALNT16 characteristically interacted with the KH3 domain of hnRNPK. j. The protein level of hnRNPK in circ-GALNT16 knockdown and overexpression cells. k. The circ-GALNT16 expression level in hnRNPK silencing cells.^nsp > 0.05, **p < 0.01