Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143.

TLDR: UCA1 can directly interact with miR-143, lower its expression and affect its downstream regulation, which constitutes a part of the oncogenic role of UCA1 in breast cancer.

Abstract: Objective Long non coding RNA (LncRNA) urothelial carcinoma-associated 1 (UCA1) is an oncogene in breast cancer. However, the detailed mechanism has not been fully revealed. This study explored whether UCA1 can directly interact with miR-143, a tumor suppressor in breast cancer and whether the UCA1-miR-143 axis is involved in regulation of cancer cell growth and apoptosis. Patients and methods miRNA microarray was performed to identify the most dysregulated miRNAs between tumor and adjacent normal tissues of breast cancer. QRT-PCR analysis was performed to assess the expression of UCA1 and miR-143. The binding between UCA1 and miR-143 was verified using dual luciferase and RNA binding protein immunoprecipitation (RIP) assay. MTT assay and flow cytometry analysis were performed to study the role of UCA1-miR-143 axis in cell proliferation, cell cycle and apoptosis. Results UC1 was significantly upregulated, while miR-143 was significantly downregulated in the tumor tissues than in the adjacent normal tissues. There are direct interactions between miR-143 and the miRNA recognition sites of UCA1. UCA1 is present in Ago2-containing RNA-induced silencing complex (RISC), through association with miR-143. Through downregulating miR-143, UCA1 can modulate breast cancer cell growth and apoptosis. Conclusions UCA1 can directly interact with miR-143, lower its expression and affect its downstream regulation. Therefore, the UCA1-miR-143 axis constitutes a part of the oncogenic role of UCA1 in breast cancer.