Abstract
Background: Triple negative breast cancer (TNBC), a fatal malignant tumor, is characterized by a lack of estrogen and progesterone hormone receptors and overexpression of HER2. Due to its characteristics, there are no effective targeted therapies for TNBC. Therefore, it is critical to identify the crucial factors that participate in modulating TNBC progression and explore the underlying molecular mechanism.Methods: CCK-8, bromodeoxyuridine incorporation, western blotting, qPCR, and transwell assays were utilized to evaluate breast cancer cell proliferation, migration, and invasion.Results: Activation of platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR) promoted the proliferation and metastatic phenotype of TNBC cells; however, these effects were attenuated by SHP-2 knockdown. Moreover, PDGF-B promoted the expression of zinc finger E-box binding homeobox 1 (ZEB1) by downregulating the expression of miR-200. Furthermore, knockdown of ZEB1 mitigated the promoting effects of PDGF-B on cell proliferation and migration. In addition, the regulatory effects of PDGF-B on miR-200 and ZEB1 were mediated through the SHP-2/Akt pathway.Conclusion: Our findings highlight the important roles of PDGF-B/PDGFR and their downstream signaling pathways in regulating cell proliferation and metastatic phenotype in TNBC. Hence, these molecules may serve as novel therapeutic targets for TNBC in the future.
Highlights
Breast cancer is one of the most common tumors among women worldwide
We aimed to investigate the relationship between Platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR) signaling and Zinc finger E-box binding homeobox 1 (ZEB1) in breast cancer cell proliferation and metastatic phenotype, as well as explore the underlying mechanisms
Our results showed that exogenous PDGF-B promoted triple negative breast cancer (TNBC) cell proliferation and metastatic phenotype, but treatment with a PDGFR inhibitor or siRNA attenuated these effects
Summary
Breast cancer is one of the most common tumors among women worldwide. The majority of cancer-induced deaths are caused by distant metastasis, the rates of metastasis and SHP-2 Participates in Regulating TNBC mortality have decreased in patients with breast cancer [3]. Certain complex mechanisms, such as epithelial-mesenchymal transition (EMT) and angiogenesis are involved in the regulation of distant metastasis [4,5,6]. Triple negative breast cancer (TNBC), a fatal malignant tumor, is characterized by a lack of estrogen and progesterone hormone receptors and overexpression of HER2. It is critical to identify the crucial factors that participate in modulating TNBC progression and explore the underlying molecular mechanism
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