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. 2021 Mar 1;40:86. doi: 10.1186/s13046-021-01890-1

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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. 8 — The schematic depiction of the positive feedback loop of HMGA1-TRIP13-c-Myc pathway. HMGA1 can induce the transcription and expression of TRIP13, therefore suppress FBXW7 expression and stabilize c-Myc, and eventually promote pCCA proliferation, migration, invasion, stemness and EMT. In the other side, c-Myc promoted HMGA1 and TRIP13 transcription, forming a positive feedback loop to amplify the effects of HMGA1-TRIP13 axis. Moreover, HMGA1 increased c-Myc expression via upregulating TCF family, which established another positive feedback pathway