Long non-coding RNA LINC00673 promotes breast cancer proliferation and metastasis through regulating B7-H6 and epithelial-mesenchymal transition.

Abstract

BACKGROUND: Long non-coding RNAs (LncRNAs) have been reported as key regulators of tumor progression in recent decades. However, the potential molecular mechanisms of breast cancer are still unclear. With the development of sequencing technology, we discovered that LINC00673 is upregulated in tumor tissues. But the main role of LINC00673 in breast cancer has yet to be confirmed. MATERIALS AND METHODS: 35 pairs of breast tumors and normal tissues were selected to real-time quantitative polymerase chain reaction (RT-qPCR) to validate LINC00673 is overexpressed in tumor tissues. We conducted proliferation, colony formation, migration, invasion assays, and EMT-related phenotype to determine the specific role of LINC00673 in breast cancer cell lines (MDA-MB-231, BT-549, and MCF-7) transfected with small interfering RNA. Gene expression profiling was conducted to found LINC00673-associated gene transcriptional changes. RESULTS: We discovered that LINC00673 is significantly upregulated in breast cancer tissues compared to paired adjacent non-tumor tissues by RT-qPCR and highly expressed LINC00673 is positively correlated with lymph node metastasis and clinical stage in the validated cohort. Knocking down LINC00673 inhibited cell proliferation and metastasis, whereas upregulated LINC00673 had the opposite effect. Gene expression profiling results indicated that LINC00673 could influence NCR3LG1(B7-H6) expression in transcriptional level. Western Blot showed us that LINC00673 could regulate epithelial-mesenchymal transition (EMT) and B7-H6 in protein level. Then we demonstrated that knocking down B7-H6 could decrease breast cancer cell proliferation and metastasis. CONCLUSION: In this study, we identified the role of LINC00673 in inducing proliferation and metastasis of breast cancer cell lines and it might act as an underlying therapeutic target for breast cancer.