Eur Rev Med Pharmacol Sci 2019; 23 (24): 10835-10841
DOI: 10.26355/eurrev_201912_19787

Long non-coding RNA TTN-AS1 promotes the metastasis in breast cancer by epigenetically activating DGCR8

P. Qiu, Y. Dou, L.-Z. Ma, X.-X. Tang, X.-L. Liu, J.-W. Chen

Department of Medical Oncology, Xingtai People’s Hospital, Xingtai, China. qiupengxt@163.com


OBJECTIVE: Breast cancer (BC) is one of the most common fatal cancers. Recent studies have identified the vital roles of long non-coding RNAs (lncRNAs) in the development and progression of BC. This research aimed to investigate the underlying mechanisms of lncRNA TTN-AS1 in the metastasis of BC.

PATIENTS AND METHODS: TTN-AS1 expression of tissues was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) in 50 BC patients. Wound healing assay and transwell assay were used to observe the phenotypic alteration of BC cells after knockdown or overexpression of TTN-AS1. Moreover, RT-qPCR and Western blot assay were performed to discover the potential targets of TTN-AS1 in BC.

RESULTS: TTN-AS1 expression in BC samples was significantly higher than that of the adjacent tissues. Besides, the migration and invasion of BC cells were markedly inhibited after TTN-AS1 was silenced, while promoted after TTN-AS1 overexpression. In addition, a remarkable decrease of DGCR8 was observed after TTN-AS1 was inhibited in BC cells, while DGCR8 was upregulated after overexpression of TTN-AS1. Furthermore, DGCR8 expression showed significant enhancement in BC tissues and was positively associated with TTN-AS1 level.

CONCLUSIONS: Our study uncovered a new oncogene in BC and suggested that TTN-AS1 could enhance BC cell migration and invasion via sponging DGCR8, which provided a novel therapeutic target for the treatment of breast cancer.

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P. Qiu, Y. Dou, L.-Z. Ma, X.-X. Tang, X.-L. Liu, J.-W. Chen
Long non-coding RNA TTN-AS1 promotes the metastasis in breast cancer by epigenetically activating DGCR8

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 24
Pages: 10835-10841
DOI: 10.26355/eurrev_201912_19787