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. 2020 Jun 1;10:8863. doi: 10.1038/s41598-020-65928-8

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© The Author(s) 2020

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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Loss of PRP3 has an inhibitory effect on cell viability and metastasis in cSCC cells. (A) PRP3 expression and the JAK2/STAT3 pathway were inhibited following PRP3 knockdown in SCC13 cells. (B) The relative protein expression of PRP3, phosphorylated JAK2 and phosphorylated STAT3. (C) The expression location of PRP3 was explored via immunofluorescence (D) CCK8 assay revealed that loss of PRP3 reduced cell proliferation. (E) Colony formation assay revealed that the loss of PRP3 inhibited the ability of colony formation. (F) Transwell assay showed that cell invasion was inhibited by PRP3 knockdown in SCC13 cells. (G) The analyze of the invaded cell number. (H) The ability of cell migration was explored via wound healing assay. ^**P < 0.01. PRP3, pre-mRNA processing factor 3.