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. 2022 Jun 1;21:121. doi: 10.1186/s12943-022-01599-5

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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 — HIF1A promotes MYH9 transcription. a-b. The expression level of HIF1A in PDAC tissues and matched noncancerous tissues was detected by qRT–PCR. Kaplan–Meier analysis was used to illuminate the correlation between the level of HIF1A and the survival time of PDAC patients. The median expression value of HIF1A was used as the cutoff (n = 49). Log-rank tests were used to determine the statistical significance. c. HIF1A knockdown and overexpression cell lines were constructed. d. GEPIA analysis showed a positive relationship between MYH9 and HIF1A in PDAC tissues. e. Correlation analysis showed a positive relationship between MYH9 and HIF1A in 97 PDAC tissues. 18 S served as the internal control. f. MYH9 mRNA expression was significantly downregulated in HIF1A-knockdown PDAC cells and upregulated in HIF1A-overexpressing PDAC cells. g. CHIP assays revealed that HIF1A could bind to two fragments (-1194 – -1185, -561 – -552) of the MYH9 promoter. h-j. Luciferase reporter assays were used to confirm the interaction between HIF1A and two fragments (-1194 – -1185, -561 – -552) of the MYH9 promoter. k. Schematic diagram illustrating the mechanism by which circSTX6 promotes PDAC proliferation and metastasis through posttranscriptional and transcriptional regulation of MYH9 by sponging miR-449b-5p and inhibiting VHL-EloBC-CUL2-Rbx1 complex-dependent ubiquitination of HIF1A, respectively. (Values are expressed as the means ± SDs; *P < 0.05, **P < 0.01 and ***P < 0.001)