GENERAL COMMENTARY article

Front. Oncol., 20 July 2021

Sec. Cancer Genetics

Volume 11 - 2021 | https://doi.org/10.3389/fonc.2021.707516

Commentary: Identification of IFN-Induced Transmembrane Protein 1 With Prognostic Value in Pancreatic Cancer Using Network Module-Based Analysis

  • 1. Department of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China

  • 2. Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, China

The human interferon (IFN)-induced transmembrane protein 1 (IFITM1), also called Leu13 or CD225, is a 17-kDa cell-surface membrane protein in the IFN-stimulated genes (ISGs) protein family (1). IFITM1 was initially identified as a leukocyte membrane surface antigen involving in signal transduction in lymphocytes, such as antiproliferative and homotypic adhesion signaling (2, 3). Additionally, IFITM1 was regarded as a modulator of immunity and antiviral activity (1). Recently, with great interest we read a study “Identification of IFN-Induced Transmembrane Protein 1 With Prognostic Value in Pancreatic Cancer Using Network Module-Based Analysis” in Frontiers in Oncology (4), revealing that the expression level of IFITM1 was increased in pancreatic cancer. Patients with IFITM1 overexpression had poor survival, and IFITM1 was one of the independent prognostic factors for overall survival. Moreover, down-regulation of IFITM1 significantly suppressed the tumorigenicity of pancreatic cancer cells (4). In addition, increasing evidence have demonstrated that IFITM1 was also upregulated in numerous tumor tissues as well as cancer cell lines, such as colorectal cancer (5), gastroesophageal adenocarcinoma (6), gastric cancer (7, 8), hepatocellular carcinoma (9), lung cancer (10), breast cancer (11, 12), head and neck cancer (13, 14), gallbladder carcinoma (15), ovarian cancer (16), glioma (17), and nasopharyngeal carcinoma (18). Overexpression of IFITM1 enhanced cell proliferation, invasion, metastasis, angiogenesis, and therapeutic resistance, including endocrine therapy, chemotherapy, and radiotherapy resistance of tumors. Mechanically, IFITM1 exerted cancer-promoting effects through regulating serval pathways, including EGFR/SOX2 (10), JAK/STAT (11), and CAV-1 (19). These findings suggest that pharmacological or genetic inhibition of IFITM1 maybe a potential and novel therapeutic approach for tumors.

Statements

Author contributions

Study concept and design, XL. Data analysis, methodology, drafting manuscript, RL. Review and editing, supervision, LY. All authors contributed to the article and approved the submitted version.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

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Summary

Keywords

IFITM1, cancer, treatment, progress, target

Citation

Li X, Liang R and Yang L (2021) Commentary: Identification of IFN-Induced Transmembrane Protein 1 With Prognostic Value in Pancreatic Cancer Using Network Module-Based Analysis. Front. Oncol. 11:707516. doi: 10.3389/fonc.2021.707516

Received

10 May 2021

Accepted

08 July 2021

Published

20 July 2021

Volume

11 - 2021

Edited by

Shilpa S. Dhar, University of Texas MD Anderson Cancer Center, United States

Reviewed by

Ken Hirasawa, Memorial University of Newfoundland, Canada

Updates

Copyright

*Correspondence: Liu Yang,

†These authors have contributed equally to this work

This article was submitted to Cancer Genetics, a section of the journal Frontiers in Oncology

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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