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. 2022 Apr 27;41:156. doi: 10.1186/s13046-022-02336-y

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© The Author(s) 2022

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. 9 — Circ_0001875/miR-31-5p/SP1 axis correlates with NSCLC prognosis and the schematic diagram illustrates the mechanism. a–c Kaplan–Meier survival curves showed the overall survival of NSCLC patients with low and high circ-0001875, miR-31-5p or SP1 expression (n = 72). d–f Correlation analysis between circ-0001875, miR-31-5p and SP1 expression analyzed by RT-qPCR in NSCLC tissues (n = 72). g Schematic diagram illustrates the mechanism by which the circ-0001875/miR-31-5p/SP1 and EMT axis promotes NSCLC proliferation and metastasis and negatively regulates by a SP1-AluSq-dependent feedback loop, but hypoxia-induced HIF1α-SP1 interaction disrupts the circ-0001875/miR-31-5p/SP1/AluSq feedback loop. The schematic diagram was elaborated by BioRender. Data are shown as the means ± SD. *p < 0.05, **p < 0.01, ***p < 0.001