Mechanism of transcription factor SPI1 regulating lung cancer cell proliferation, invasion and migration by targeting EXO1

To investigate the mechanism of transcription factor SPI1 regulating lung cancer cell proliferation, invasion and migration by targeting EXO1. Relevant data were from the TCGA database and GEO database. Kaplan-Meier curves were plotted to analyze the overall survival time. The expression level of EXO1 and SPI1 was verified by qRT-PCR and Western blotting. And colony formation, cell scratch, and Transwell were used to evaluate the effects of EXO1 and SPI1. Western blotting was used to detect the expression changes of epithelial-mesenchymal transition (EMT)-related proteins and the Wnt/β-catenin signaling pathway. The transcription factor of EXO1 was predicted by the UCSC database and verified by dual-luciferase assay. EXO1 was significantly upregulated in lung cancer with high EXO1 expression had a shorter overall survival time than those with low EXO1 expression. Silencing EXO1 inhibited the phenotype of lung cancer cells. The UCSC database prediction and dual-luciferase assay showed that the transcription factor SPI1 could regulate the expression of EXO1. Additionally, SPI1 was lowly expressed in lung cancer patients, and lung cancer patients with low SPI1 expression had a lower overall survival rate than those with high SPI1 expression. Overexpression of SPI1 inhibited the phenotype of lung cancer cells, promoted the expression of E-cadherin, and inhibited the expression of N-cadherin, Snail, and β-catenin, while overexpression of EXO1 could reverse the inhibitory effect of SPI1 overexpression on lung cancer cells. Transcription factor SPI1 regulates the proliferation, invasion, and migration of lung cancer cells by targeting EXO1.