LncRNA MORT negatively regulates FGF1 to suppress malignant progression of breast cancer

Q. Yang, D. Yang, H.-B. Zhu, P. Li, X.-P. Wu, Y.-R. Tan

Department of Oncology Radiotherapy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China. tanyeru@163.com

 

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• Oncology

OBJECTIVE: To explore the biological function of long non-coding RNA (lncRNA) MORT in the malignant progression of breast cancer (BCa) and the underlying mechanism, and to provide a novel strategy for clinical treatment.

PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect differential level of MORT in BCa specimens and cell lines. The correlation between MORT level and pathological indexes of BCa patients was analyzed. After intervening MORT level in SKBR-3 and MCF-7 cells, cell viability, migratory rate and wound closure were examined through Cell Counting Kit-8 (CCK-8), transwell and wound healing assay, respectively. Dual-Luciferase reporter assay and rescue experiments were conducted to uncover the regulatory effect of MORT on its target gene FGF1. In vivo function of MORT in mediating tumor growth of BCa was finally assessed by generating a xenograft model in nude mice.

RESULTS: MORT was downregulated in BCa tissues and cell lines. Low level of MORT predicted higher rate of distant metastasis in BCa patients. Overexpression of MORT in SKBR-3 cells reduced proliferative and migratory rates, while knockdown of MORT in MCF-7 enhanced them. Moreover, in vivo overexpression of MORT slowed down tumor growth of BCa in nude mice. MORT could negatively regulate its target gene FGF1, which was responsible for the anti-cancer role of MORT in BCa progression.

CONCLUSIONS: MORT is downregulated in BCa specimens, which suppresses proliferative and migratory potentials of BCa cells by negatively regulating FGF1. MORT can be an effective target for precision treatment of BCa.

 

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