OPN3 enhances the proliferation, migration, and invasion of triple-negative breast cancer cells via the regulation of the TGF-β signaling pathway

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Background: Opsin3 (OPN3) belongs to the guanine nucleotide-binding protein-coupled receptor superfamily, implicated in several pathological mechanisms that contribute to tumor development and resistance to treatment. This study examined OPN3 expression in triple-negative breast cancer (TNBC) tissues and its function in TNBC cell propagation, invasion, and migration. Methods: The study analyzed OPN3 expression in TNBC patients and its diagnostic value using immunohistochemistry (IHC) staining and The Cancer Genome Atlas (TCGA) data. To evaluate the impact of OPN3 on the growth, invasion, and migration of TNBC cells, both in vitro and in vivo experiments were carried out. The biological mechanisms of OPN3-induced cell migration and invasion were evaluated via quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) analyses. Results: In this study, OPN3 upregulation in TNBC tissues was found to be correlated with decreased overall survival (OS) and progression-free survival (PFS) rates. The propagation, invasion, and migration of BT-549 cells were promoted and apoptosis was reduced after OPN3 overexpression. It was silenced in BT-549 cells, which resulted in the opposite effects. Further, the transforming growth factor-beta (TGF-β)/SMAD2 signaling pathway was stimulated and the epithelial-mesenchymal transition (EMT) was modulated by OPN3 overexpression in BT-549 cells. Conclusions: The findings revealed that OPN3 is involved in the stimulation of the TGF-β/SMAD2 signaling pathway, which promotes the growth, migration, and dissemination of TNBC cells. Moreover, OPN3 can serve as a diagnostic biomarker and a treatment target for TNBC.

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