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

Y.-L. Tuo, X.-M. Li, J. Luo

Department of Breast Surgery, Sichuan Provincial People’s Hospital, School of Clinical Medicine of University of Electronic Science and Technology of China, Chengdu, China. jingluo66@sina.com

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• Oncology

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.

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