RESUMEN
Cancer is a genetic and complex disorder, resulting from several events associated with onset, development, and metastasis. Tumor suppressors and oncogenes are among the main regulators of tumor progression, contributing to various cancer-related behaviors like cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), cell cycle, and apoptosis. Transcription factors (TFs) could act as tumor suppressors or oncogenes in cancer progression. E-twenty-six/E26 (ETS) family of TFs have a winged helix-turn-helix (HLH) motif, which interacted with specific DNA regions with high levels of purines and GGA core. ETS proteins act as transcriptional repressors or activators to modulate the expression of target genes. ETS transcription factor ELK3 (ELK3), as a type of ETS protein, was shown to enhance in various cancers, suggesting that it may have an oncogenic role. These studies indicated that ELK3 promoted invasion, migration, cell cycle, proliferation, and EMT, and suppressed cell apoptosis. In addition, these studies demonstrated that ELK3 could be a promising diagnostic and prognostic biomarker in human cancer. Moreover, accumulating data proved that ELK3 could be a novel chemoresistance mediator in human cancer. Here, we aimed to explore the overall change of ELK3 and its underlying molecular mechanism in human cancers. Moreover, we aimed to investigate the potential role of ELK3 as a prognostic and diagnostic biomarker as well as its capability as a chemoresistance mediator in cancer.
