Long non-coding RNA FOXD2-AS1 functions as a tumor promoter in colorectal cancer by regulating EMT and Notch signaling pathway
X. Yang, B. Duan, X. Zhou Department of Pathophysiology, Basic Medical Science, Shanxi Medical University, Taiyuan, Shanxi, China. zxhi555@163.com
OBJECTIVE: A growing number of long noncoding RNAs (lncRNAs) are emerging as new modulators in cancer origination and progression. However, the functions and molecular mechanisms of lncRNAs to colorectal cancer (CRC) are still largely unknown. The aim of this study was to investigate the function and role of lncRNA FOXD2-AS1 (FOXD2-AS1) in human CRC.
PATIENTS AND METHODS: The expression of FOXD2-AS1 was investigated using Real-time reverse transcription-polymerase chain reaction (qRT-PCR) in 45 CRC specimens and matched adjacent normal tissues and CRC cell lines. MTT assays were conducted to explore the impact of FOXD2-AS1 knockdown on the proliferation of human CRC cells. The effects of FOXD2-AS1 on CRC cell migration and invasion were evaluated by cell invasion assays and migration assays. Western blot analysis was used to determine the expression levels of EMT-related and Notch-related proteins.
RESULTS: The results showed that FOXD2-AS1 expression was significantly increased in CRC tissues as well as in CRC cell lines. Moreover, down-regulation of FOXD2-AS1 suppressed cell, proliferation, invasion and migration in vitro. Importantly, we further confirmed that EMT and the Notch signaling pathway were inactivated in CRC cells after FOXD2-AS1 knockdown.
CONCLUSIONS: FOXD2-AS1 promoted the progression of CRC by regulating EMT and Notch signaling pathway. Thus, targeting FOXD2-AS1 may be an effective strategy for CRC treatment.
Free PDF DownloadThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License
To cite this article
X. Yang, B. Duan, X. Zhou
Long non-coding RNA FOXD2-AS1 functions as a tumor promoter in colorectal cancer by regulating EMT and Notch signaling pathway
Eur Rev Med Pharmacol Sci
Year: 2017
Vol. 21 - N. 16
Pages: 3586-3591
DOI: 10.26355/eurrev_201708_13269