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. 2022 Mar 29;8:140. doi: 10.1038/s41420-022-00948-z

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — miR-31 exerts its central roles in OSCC by constituting a complex network with the direct target genes (e.g. RhoA, FIH, ACOX1, VEGF, SIRT3, LATS2, KANK1, and NUMB) and the signaling cascades (e.g. ERK-MMP9 cascade, Hippo pathway, Wnt signaling, and MCT1/MCT4 regulatory cascade). RhoA= ras homolog family member A; EMT = epithelial-to-mesenchymal transition; FIH = factors inhibiting HIF; hTERT = human telomerase reverse transcriptase; VEGF = vascular endothelial growth factor; PGE2 = prostaglandin E2; ACOX1 = acyl-CoA oxidase 1; ROS = reactive oxygen species; SIRT3 = silent information regulator 3; LATS2 = large tumor suppressor kinase 2; KANK1 = KN motif and ankyrin repeat domain-containing protein 1; CASC2 = long non-coding RNA cancer susceptibility candidate 2; WLS = wntless; NUMB = NUMB endocytic adaptor protein.