scholarly journals Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines

10.3791/54350 ◽  
2016 ◽  
Author(s):  
Brianna C. Morten ◽  
Rodney J. Scott ◽  
Kelly A. Avery-Kiejda
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines

scholarly journals INHBA Promotes Cell Proliferation and Metastasis of Breast Cancer through Wnt/β-catenin Signaling Pathway

2021 ◽  
Author(s):  
Tao Xueqin ◽  
Mei Jinhong ◽  
Huang Yuping
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
The Cancer Genome Atlas ◽  
Breast Cancer Cell Lines ◽  
Mesenchymal Transition

Abstract BackgroundEmerging evidences have demonstrated that inhibin subunit beta A (INHBA) is dysregulated and play critical roles in various cancers. With the development of sequencing technology, studies have discovered that INHBA is overexpressed in breast cancer tissues. However, the biological roles of INHBA in breast cancer are still far to clear. In the present study, MethodsWe analyzed the INHBA expression in the Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of INHBA in breast cancer cell lines. Cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were determined by using CCK-8, EdU, Transwell and western blot assays.ResultsINHBA was highly expressed in breast cancer cell lines. Functional analysis revealed that silence or elevation of INHBA inhibited or promoted the proliferation, migration, invasion and EMT and Wnt/β-catenin signaling pathway related markers of MCF-7 cells. Mechanically, blocking of Wnt/β-catenin pathway by XAV939 reversed the promotion effect of INHBA overexpression on breast cancer cells’ proliferation, migration and invasion.ConclusionOur findings emphasized that INHBA may act as an oncogene via activating the Wnt/β-catenin pathway, which may provide a potential therapeutic target for the treatment of breast cancer.

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