Abstract

The objective of the study was to explore the role of SDC1 in breast cancer cells. Our study also investigated the regulatory relationship between SDC1 and the microRNA (miRNA) miR-335-5p as well as the impact of these two genes on the progression of breast cancer. Bioinformatic approaches were employed to analyze the differentially expressed messenger RNAs (mRNAs) and miRNAs (DE-mRNAs and DE-miRNAs) in breast cancer tissue. Then mRNA SC1 was obtained. Differentially downregulated mRNAs were intersected with target miRNAs predicted by databases, and miR-335-5p was determined as the study object. Quantitative reverse transcription polymerase chain reaction was applied to assess the expressions of SDC1 and miR-335-5p in each cell line. Next, Western blot assay was conducted to detect the protein level of SDC1 and dual-luciferase assay was performed to verify the binding relationship between miR-335-5p and SDC1. Finally, we conducted methyl thiazolyl tetrazolium (MTT), colony formation, and Transwell assays and flow cytometry to further investigate the impacts of SDC1 and miR-335-5p on the progression of breast cancer. SDC1 was significantly highly expressed while miR-335-5p was remarkably lowly expressed in human breast cancer. Silencing SDC1 in breast cancer blocked the proliferation, migration and invasion of the cells. In breast cancer, SDC1 was a target gene of miR-335-5p and silencing miR-335-5p notably increased SDC1 expression. Compared with the silence of miR-335-5p, simultaneous silences of miR-335-5p and SDC1 significantly reduced the proliferative, migratory and invasive abilities of breast cancer cells. The result revealed the interaction between miR-335-5p and SDC1 in the progression of breast cancer, which may contribute to the treatments for this cancer.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.