Egr-1 inhibits colon cancer cell proliferation, migration and invasion via regulating CDKL1 at the transcriptional level

Colon cancer is one of the most common malignant tumors worldwide, and the molecular mechanisms involved in the oncogenesis and progression of colon cancer remain unclear. Early growth response 1 (Egr-1) is a transcription factor that is closely associated with several tumor processes; however, its role in colon cancer is unknown. The present study aimed to explore the function and mechanism of transcription factor Egr-1 in colon cancer progression. The association between Egr-1 expression and the survival of patients with colon cancer was analyzed. Transwell assay was used to measure the migration and invasion of colon cancer cells. Cell Counting Kit-8 assay was used to evaluate the cell proliferative ability. Reverse transcription-quantitative PCR and western blot assays were used to identify whether Egr-1 could regulate cyclin-dependent kinase-like 1 (CDKL1). Luciferase and chromatin immunoprecipitation assays were used to detect the mechanism by which Egr-1 regulated CDKL1. Based on The Cancer Genome Atlas database, it was found that low Egr-1 expression was associated with a poor prognosis in patients with colon cancer. Furthermore, overexpression of Egr-1 inhibited colon cancer cell proliferation, migration, and invasion, whereas knockdown of Egr-1 increased colon cancer cell proliferation, migration and invasion. Additionally, overexpression of Egr-1-induced cell proliferation, migration and invasion were reversed by overexpression of CDKL1. Furthermore, it was demonstrated that Egr-1 regulated CDKL1 expression at the transcriptional level. The present study illustrated the mechanism of Egr-1 regulating CDKL1, by which Egr-1 affected colon cancer cell proliferation, migration and invasion. The current findings suggested that Egr-1/CDKL1 may be a new promising target for the treatment of colon cancer.