Downregulation of Dock1 and Elmo1 suppresses the migration and invasion of triple-negative breast cancer epithelial cells through the RhoA/Rac1 pathway.

Dedicator of cytokinesis 1 (Dock1), a guanine nucleotide exchange factor, has been proven to facilitate cell survival, motility and proliferation via the activation of Ras-related C3 botulinum toxin substrate 1 (Rac1). Engulfment and cell motility 1 (Elmo1) serves as a mammalian homolog of Ced-12, which has been evolutionarily conserved from worm to human. The present study aimed to investigate the roles and mechanisms of Dock1 and Elmo1 in the migration and invasion of triple-negative breast cancer (TNBC) epithelial cells. Cell Counting kit-8, cell migration and cell invasion assays were performed to assess cell viability, migration and invasion, respectively. A plate clone formation assay was performed to determine cell proliferation. Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays were used to evaluate mRNA and protein expression. The results revealed that the downregulation of Dock1 and Elmo1 inhibited cell viability, suppressed migration and invasion, and reduced Rac1 activity in MDA-MB-231 cells. Furthermore, downregulation of Dock1 and Elmo1 also attenuated the expression of migration-associated proteins and affected the Ras homolog gene family, member A (RhoA)/Rac1 pathway in MDA-MB-231 cells. In conclusion, the results of the present study suggested that the downregulation of Dock1 and Elmo1 suppresses the migration and invasion of TNBC epithelial cells through the RhoA/Rac1 pathway.