Abstract
BackgroundResistance to human epidermal growth factor receptor-2 (HER2)-targeted therapies is common, and results in treatment failure and new tumor progression. C35 is over-expressed in many invasive breast cancer endogenously, and functions as an oncogene in breast cancer cell lines.MethodsThe current study aims to investigate effects of C35 on cell viability and migration of HER2-positive breast tumor cells and explore possible mechanisms. The protein expression of C35 in BT-474 breast ductal carcinoma cells was interfered by siRNAs. MTT assay was utilized to detect the viability of BT474 breast ductal carcinoma cells after transfection. The migration of BT474 breast ductal carcinoma cells was examined by cell wound scratch assay.ResultsIn addition, the protein expression of C35, HER2, AKT and p-AKT in breast ductal carcinoma cells were detected by Western Blot. The protein expression of C35 was weaker in siRNA1 and siRNA2 groups compared with the control group. The relative expression ratio of C35 to β-actin decreased significantly in siRNA2 and siRNA1 groups. When C35 expression was interfered by siRNA1 and siRNA2 for 48 h, the viability of BT474 breast ductal carcinoma cells decreased compared with the control group. In addition, the migration of breast ductal carcinoma cells decreased when C35 expression was interfered by siRNA1 for 24 h, and interfered by siRNA1 and siRNA2 for 48 h.
Highlights
Breast cancer is the most common invasive cancer in women, and it affects about 12% of women worldwide [1]
The protein expression of C35, human epidermal growth factor receptor-2 (HER2), AKT and p-AKT in breast ductal carcinoma cells were detected by Western Blot
When C35 expression was interfered by siRNA1 and siRNA2 for 48 h, the viability of BT474 breast ductal carcinoma cells decreased compared with the control group
Summary
Breast cancer is the most common invasive cancer in women, and it affects about 12% of women worldwide [1]. Human epidermal growth factor receptor-2 (HER2)-positive breast cancers are generally more aggressive than HER2-negative breast cancers [2]. HER2-targeted therapies have improved the prognosis of HER2-positive breast cancer over the last few years [3]. Resistance to the therapies is common, which results in treatment failure and new tumor progression [4]. Exploring new therapeutic approaches to treat HER-positive breast cancers is highly needed. Resistance to human epidermal growth factor receptor-2 (HER2)-targeted therapies is common, and results in treatment failure and new tumor progression. C35 is over-expressed in many invasive breast cancer endogenously, and functions as an oncogene in breast cancer cell lines.
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