Background
Breast cancer (BC) has deleterious effects on women's health worldwide, yet its molecular mechanism remains unclear.
Conclusion
This research revealed that miR-1298-5p could influence the malignancy phenotypes of BC cells by inhibiting CXCL11.
Methods
Microarray analysis was performed to identify the key mRNA and miRNA involved in BC. The expression of miR-1298-5p and CXCL11 mRNA in BC clinical tissues and cell lines was detected using quantitative reverse transcription PCR (RT-qPCR), while the demonstration of intra- and extra-cellular CXCL11 protein was measured using western-blotting or ELISA assay. CCK-8, BrdU ELISA, colony formation, wound healing, and cell adhesion assays were carried out to determine cell viability, cell proliferation, colony formation, cell migration and adhesion phenotypes, respectively. A dual-luciferase assay kit was also employed to confirm the predicted binding scheme between miR-1298-5p and CXCL11.
Objective
This study aimed to discover the underlying mechanism used by miR-1298-5p to regulate CXCL11 in BC.
Results
Microarray analysis confirmed miR-1298-5p and CXCL11 as the miRNA and mRNA to be further investigated in BC. After observing low-level miR-1298-5p and high-level CXCL11 in BC clinical tissues and cell lines, it was discovered that miR-1298-5p inhibited the phenotypes of BC cells, while CXCL11 promoted the tumorigenesis of BC cells. Findings indicated that miR-1298-5p attenuated the promotive effect of CXCL11 on BC cell phenotypes.