Long non‑coding RNA 00152 functions as a competing endogenous RNA to regulate NRP1 expression by sponging with miRNA‑206 in colorectal cancer
Autor: | Feng He, Jianchang Wei, Jie Cao, Ping Yang, He Hu, Qiang Wang, Zhuanpeng Chen, Wanglin Li, Hua‑Cui Chen, Junbin Zhong |
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Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine Cancer Research Epithelial-Mesenchymal Transition Mice Nude Kaplan-Meier Estimate Biology Metastasis Mice 03 medical and health sciences 0302 clinical medicine Cell Movement Cell Line Tumor microRNA medicine Animals Humans Gene silencing Neoplasm Invasiveness RNA Small Interfering neoplasms Cell Proliferation Oncogene Competing endogenous RNA Cancer Middle Aged medicine.disease Xenograft Model Antitumor Assays Neuropilin-1 digestive system diseases Long non-coding RNA Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Oncology 030220 oncology & carcinogenesis Cancer cell Disease Progression Mutagenesis Site-Directed Cancer research Female RNA Long Noncoding Colorectal Neoplasms |
Zdroj: | International Journal of Oncology. |
ISSN: | 1791-2423 1019-6439 |
DOI: | 10.3892/ijo.2018.4451 |
Popis: | Colorectal cancer (CRC) is the third most common type of cancer; however, the molecular mechanisms underlying colorectal tumor metastasis and growth remain elusive. Recently, accumulating evidence has indicated that long non‑coding RNAs (lncRNAs) play a critical role in CRC progression and metastasis; however, the biological role and clinical significance of lncRNA 00152 (lnc00152) in CRC remains largely unknown. Thus, in this study, lnc00152 expression was measured in 80 human CRC tissue samples, 40 non‑cancerous tissue samples, and 3 CRC cell lines (SW480, SW620 and LoVo) using RT‑qPCR. We examined the effects of lnc00152 on CRC cells following transfection with lnc00152 overexpression plasmid or respective siRNA in vitro and in vivo. Luciferase assays revealed the mechanism driving competitive endogenous RNA (ceRNA). We identified that lnc00152 was aberrantly overexpressed in colorectal tumors and cancer cells and that lnc00152 was modulated by miRNA‑206. lnc00152 overexpression enhanced the proliferative and invasive ability of CRC cells in vitro, promoted tumor growth in vivo, and was associated with the shorter overall survival of patients with CRC. In addition, lnc00152 overexpression promoted epithelial-mesenchymal transition (EMT) and increased neuropilin‑1 (NRP1) expression in the CRC cells. By contrast, lnc00152 silencing exerted a counteractive effect. Collectively, these findings demonstrate the critical role of lnc00152 in tumor growth and progression in CRC, and identify a novel therapeutic target associated with CRC development and progression. |
Databáze: | OpenAIRE |
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