Background and Aims Interferon-induced transmembrane protein 1 (IFITM1), a membrane complex transducing homotypic adhesion signals in lymphocytes, is abnormally expressed in pancreatic cancer tissues, but its action mechanism in pancreatic cancer remains unclear. Therefore, this study was conducted as a preliminary investigation to examine the influences of the expression of IFITM1 on biological behaviors of pancreatic cancer cells.Methods The expressions of IFITM1 in the surgical specimens of cancer tissue and adjacent normal tissue from 78 pancreatic cancer patients (32 cases having metastasis, 46 cases not having metastasis) were determined by Western blot analysis. In pancreatic cancer PANC-1 cells after transfection with IFITM1-overxpression plasmids alone (IFITM1 group) or with simultaneous addition of ERK_1/2 pathway inhibitor LY3214996 (IFITM1+LY3214996 group), with untreated PANC-1 cells as control group, the changes in levels of IFITM1 protein and ERK_1/2 protein phosphorylation (ERK_1/2/p-ERK_1/2), proliferative viability and apoptosis as well as migration and invasion abilities were determined by Western blot, CCK-8 assay, flow cytometry, Scratch healing assay and Transwell assay, respectively.Results The relative expression level of IFITM1 protein in pancreatic cancer tissue was significantly higher than that in adjacent normal tissue, and in pancreatic cancer tissue with metastasis was higher than that in pancreatic cancer tissue without metastasis (both P<0.05). Compared with PANC-1 cells in control group, the PANC-1 cells in IFITM1 group showed significantly increased IFITM1 protein and ERK_1/2/p-ERK_1/2 levels, decreased apoptosis rate, increased proliferative viability and enhanced migration and invasion abilities (all P<0.05); except the up-regulated IFITM1 protein level (P<0.05), the PANC-1 cells in IFITM1+LY3214996 group showed no significant changes in all other studied parameters (all P>0.05)Conclusion IFITM1 expression is increased in pancreatic cancer tissue, which is closely related to the malignant behaviors of pancreatic cancer. The mechanism may be possibly associated with its regulating the growth, migration and invasion abilities of the pancreatic cancer cells via phosphorylating and activating the ERK_1/2 pathway.