ERBB4 promotes the progression of inflammatory breast cancer through regulating PDGFRA.

Background: The regulatory roles of human epidermal growth factor receptor [erb-b2 receptor tyrosine kinase 4 (ERBB)] family in tumors was received widespread attention. Although ERBB4 was crucial regulator in metastasis of malignant tumors, the exact mechanism of ERBB4 in inflammatory breast cancer (IBC) remains unclarified.
Methods: In this study, we collected IBC tissues and cell lines, and explored the expression levels of ERBB4 and platelet-derived growth factor receptor alpha (PDGFRA) using real-time quantitative polymerase chain reaction (RT-PCR), immunohistochemistry (IHC) and western blot assays. Furthermore, cell viability with ERBB4 silencing in SUM149 cells was examined by MTT assay and cell migration and invasion were detected by transwell assay.
Results: The data indicated thatERBB4abolishing dramatically depressed capacity of proliferation, migration and invasion of IBC cells. Moreover, PDGFRA was an important factor for the function of ERBB4 and PDGFRA overexpression could, at least, partly rescue the ERBB4 silencing-mediated inhibition in proliferation and metastasis of IBC cells.
Conclusions: Take together, we verified the first time that ERBB4 promoted the progression of IBC through regulating PDGFRA. Thus, inhibition of ERBB4 might be a novel therapeutic candidate against IBC.
Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/tcr-19-2132). The authors have no conflicts of interest to declare.
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