MYCL promotes the progression of triple-negative breast cancer by activating the JAK/STAT3 pathway

Abstract

The present study aimed to investigate the underlying regulatory mechanism of MYCL proto-oncogene (MYCL) in triple-negative breast cancer (TNBC) progression. In vitro experiments were performed to confirm the functional roles of MYCL in TNBC, and its effects on the JAK/STAT3 pathway through flow cytometric analysis, colony formation, wound healing and Transwell assays. In addition, the GSE45498 dataset demonstrated that MYCL was upregulated in TNBC and that it was significantly related to poor survival of patients with TNBC. Knockdown of MYCL induced the apoptosis, and suppressed the proliferation, migration and invasion of TNBC cells by inhibiting the JAK/STAT3 pathway. Notably, MYCL could activate the JAK/STAT3 pathway, whereas inhibition of the JAK/STAT3 pathway could eliminate the effect of MYCL on TNBC cells. Knockdown of MYCL also suppressed the growth of TNBC xenograft tumors. In conclusion, MYCL could promote TNBC progression by activating the JAK/STAT3 pathway.