Abstract
ObjectivesPreviously, Interferon-induced Protein with Tetratricopeptide Repeats 1 (IFIT1) has been shown to promote cancer development. Here, we aimed to explore the role of IFIT1 in the development and progression of pancreatic cancer, including the underlying mechanisms.MethodsWe explored IFIT1 expression in pancreatic cancer samples using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Cell Counting Kit-8 (CCK8), colony formation, scratch wound-healing and Transwell assays were performed to assess the proliferation, migration and invasion abilities of pancreatic cancer cells. Gene Set Enrichment Analysis (GSEA) and Western blotting were performed to assess the regulatory effect of IFIT1 on the Wnt/β-catenin pathway.ResultsWe found that upregulation of IFIT1 expression is common in pancreatic cancer and is negatively associated with overall patient survival. Knockdown of IFIT1 expression led to decreased proliferation, migration and invasion of pancreatic cancer cells. We also found that IFIT1 could regulate Wnt/β-catenin signaling, and that a Wnt/β-catenin agonist could reverse this effect. In addition, we found that IFIT1 can promote epithelial-mesenchymal transition (EMT) of pancreatic cancer cells.ConclusionsOur data indicate that IFIT1 increases pancreatic cancer cell proliferation, migration and invasion by activating the Wnt/β-catenin pathway. In addition, we found that EMT could be regulated by IFIT1. IFIT1 may serve as a potential therapeutic target for pancreatic cancer.
Highlights
To determine Interferon-induced Protein with Tetratricopeptide Repeats 1 (IFIT1) expression in pancreatic cancer, we referred to the The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) (GSE16515, GSE15471) and Genotype-Tissue Expression (GTEx) databases and extracted information from the expression profiles of the datasets
We found that the expression level of IFIT1 in the pancreatic cancer tissues was significantly increased compared to that in the normal tissues in all these datasets (Fig. 1A-C)
By comparing the H-scores, we found that the protein levels of IFIT1 were significantly increased in pancreatic cancer samples (p = 0.01; Fig. 1D-F)
Summary
Interferon-induced Protein with Tetratricopeptide Repeats 1 (IFIT1) has been shown to promote cancer development. We aimed to explore the role of IFIT1 in the development and progression of pancreatic cancer, including the underlying mechanisms. Cell Counting Kit-8 (CCK8), colony formation, scratch wound-healing and Transwell assays were performed to assess the proliferation, migration and invasion abilities of pancreatic cancer cells. Gene Set Enrichment Analysis (GSEA) and Western blotting were performed to assess the regulatory effect of IFIT1 on the Wnt/βcatenin pathway. Results We found that upregulation of IFIT1 expression is common in pancreatic cancer and is negatively associated with overall patient survival. Knockdown of IFIT1 expression led to decreased proliferation, migration and invasion of pancreatic cancer cells. We found that IFIT1 can promote epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. Conclusions Our data indicate that IFIT1 increases pancreatic cancer cell proliferation, migration and invasion by activating the Wnt/β-catenin pathway. IFIT1 may serve as a potential therapeutic target for pancreatic cancer
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