Targeting friend leukemia integration 1: A promising approach for prevention and treatment of solid tumors

Abstract

Friend leukemia integration 1 (FLI1) is an ETS transcription factor first identified in erythroleukemia. This protein contributes to various cellular functions such as cell growth and proliferation, apoptosis, angiogenesis, etc. FLI1 is also known to be involved in tumorigenesis. The role of this transcription factor as a proto-oncogene, promoting cancer progression, especially Ewing sarcoma, is well reported. Recent research has found the connection of FLI1 with other solid cancers, including breast cancer, prostate cancer, glioma, and lung cancer. The role of this protein in solid cancers is also controversial. FLI1 is found to promote and suppress cancer growth and progression, particularly in Ewing sarcoma and breast cancer. This review article aims to provide a detailed perception of the FLI1-associated mechanisms in various solid cancers for preventive and therapeutic implications. The result of bioinformatic analysis using the cBioportal database (https://www.cbioportal.org/) is also presented in this article to understand the effect of this protein on solid cancers. Moreover, the current status of FLI1 targeting agents for preventing and treating solid cancers has been focused. Several studies established the efficacy of FLI1 inhibitors in solid tumor therapy. A few reports are also available on the effect of FLI1 agonists on solid tumors. This article discussed different FLI1 targeting agents to provide insight into the FLI1 targeting mechanisms required for discovering more potent FLI1 targeting agents and better therapeutic outcomes.

Keywords: Ewing sarcoma; FLI1; Inhibitor; Prevention; Solid cancer; Targeting; Therapy.