Abstract
Interferon-induced transmembrane protein 1 (IFITM1) has been shown to be implicated in multiple cancers, yet little is known about biological significance of IFITM1 in colorectal cancer. Here, we show that IFITM1 is highly expressed in metastatic colorectal cancer cell lines as well as colorectal patient-derived tumor samples, and its expression is associated with a poor prognosis of the disease. Also, IFITM1 depletion resulted in a significant reduction in the mobility of cancer cell lines, whereas ectopic expression of IFITM1 promoted the migration of cancer cells. Epithelial-mesenchymal transition (EMT) signature was dysregulated by both loss and gain of function of IFITM1, which was partially reverted by Caveolin-1 (CAV1). Therefore, these results suggest that IFITM1 may be a prognostic marker and an attractive target to achieve better therapeutic outcomes in colorectal cancer.
Highlights
Colorectal cancer (CRC), the third most common type of cancer in the world, is one of the leading causes of cancer deaths with a worldwide incidence of more than one million cases per year [1,2,3,4,5]
We show that Interferon-induced transmembrane protein 1 (IFITM1) is highly expressed in metastatic colorectal cancer cell lines as well as colorectal patient-derived tumor samples, and its expression is associated with a poor prognosis of the disease
As IFITM1 has been shown to be increased in cervical, esophageal, ovarian, brain and colon cancers [27,28,29,30,31], we analyzed the expression of IFITM1 in multiple patient-derived colorectal cancer cell lines by immunoblot
Summary
Colorectal cancer (CRC), the third most common type of cancer in the world, is one of the leading causes of cancer deaths with a worldwide incidence of more than one million cases per year [1,2,3,4,5]. CRC develops and progresses over several years with distinct molecular and cytological characteristics, eventually resulting in a carcinoma with a high rate of invasion and metastasis [3, 6]. Despite recent advances in the screening, surgical resection, systemic chemotherapies, and treatment modalities of CRC, which led to a higher rate of response and better quality of life, most of the key signaling pathways involved in its progression still need to be identified and characterized. EMT is known to be implicated in many important events such as invasion, tumor progression, resistance to chemotherapy and the acquisition of stem cell-like characteristics [13,14,15,16,17,18,19,20]. The cross talk of these signaling pathways and their novel components requires to be characterized to understand the role of EMT in tumor progression
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