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. 2021 Jun 28;12(7):656. doi: 10.1038/s41419-021-03938-8

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© The Author(s) 2021

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. 6 — COL11A1 was upregulated in pancreatic cancer tissues and overexpression of COL11A1 promotes cancer progression. COL11A1 expression in pancreatic cancer and adjacent normal tissues were analyzed in multiple Gene Expression Omnibus (GEO) datasets (A) and our own cohort (B). C Expression of COL11A1 in pancreatic cancer tissues and adjacent non-tumor tissues was detected by western blot. D Kaplan–meier analysis was used to analyze the relationship between COL11A1 expression and prognosis of pancreatic cancer in TCGA dataset. E, F Representative IHC staining of COL11A1 and the distribution of COL11A1 staining intensity in pancreatic cancer tissues and non-tumor control tissues. Scale bars, 200 μm. G Kaplan–Meier survival analysis of survival rate between pancreatic cancer patients with low or high COL11A1 expression. H Western blot analysis of COL11A1 expression in SW1990 or PANC-1 cells transfected with negative control (sh-NC), or lentivirus targeting COL11A1 (sh- COL11A1). Cell proliferation capability of SW1990 or PANC-1 cells transfected with sh-NC or sh- COL11A1 was determined by CCK-8 assay (I), colony formation assay (J) in vitro, and tumor xenografts experiment (K) in vivo. Cell proliferation capability of SW1990 or PANC-1 cells transfected with sh-NC or sh- COL11A1 was determined by CCK-8 assay (I), colony formation assay (J) in vitro, and tumor xenografts experiment (K) in vivo. Metastasis capability of pancreatic cancer cells after COL11A1 silencing was determined by transwell assay (L) in vitro, and intravenous pulmonary metastasis experiment (M) in vivo. The results are presented as the mean ± SD for each group (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001.