Down-regulation of C35 decreased the cell viability and migration of breast ductal carcinoma cells.

ABSTRACT:

Background

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.

Methods

The 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.

Results

In addition, the protei

SUBMITTER: Che W 

PROVIDER: S-EPMC5578656 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature