LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway

Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the express...

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Veröffentlicht in:Molecular medicine reports 2018-08, Vol.18 (2), p.2269-2276
Hauptverfasser: Jing, Niancai, Huang, Tao, Guo, Huaiyu, Yang, Jili, Li, Mingjing, Chen, Zhuo, Zhang, Yue
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Sprache:eng
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Zusammenfassung:Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor‑Node‑Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)‑4310 that targeted LGR5. Through the inhibition of miR‑4310, CASC15 promoted leucine‑rich repeat‑containing G‑protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/β‑catenin signaling pathway. The results revealed that the inhibition of the Wnt/β‑catenin signaling pathway in CASC15‑overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/β‑catenin signaling pathway in a miR‑4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.
ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2018.9191