Long non‑coding RNA ATB is associated with metastases and promotes cell invasion in colorectal cancer via sponging miR‑141‑3p
- Xianming Liu
- Cunchuan Wang
Affiliations: Department of Gastrointestinal Surgery, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen, Guangdong 518020, P.R. China, Department of Gastrointestinal Surgery, Guangzhou Overseas Chinese Hospital, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China
- Published online on: October 27, 2020 https://doi.org/10.3892/etm.2020.9391
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Long non‑coding RNAs (lncRNAs) serve crucial roles in cancer development and progression. lncRNA‑activated by transforming growth factor‑β (lncRNA‑ATB) mediates cell proliferation. However, the association between lncRNA‑ATB and human colorectal cancer (CRC) is not completely understood. Therefore, the present study aimed to investigate the role of lncRNA‑ATB in CRC, as well as the underlying mechanism. 50 pairs of tumor tissues and adjacent normal tissues from patients with primary CRC were collected. The expression of lncRNA‑ATB and microRNA (miR)‑141‑3p in CRC tissues, adjacent normal tissues and cell lines was detected using reverse transcription‑quantitative PCR. CCK‑8, colony formation, Transwell, western blot, dual luciferase reporter gene, RNA immunoprecipitation and immunohistochemistry staining assays were conducted to assess the biological function of lncRNA‑ATB and miR‑141‑3p in CRC progression. lncRNA‑ATB was upregulated in CRC tissues and cell lines compared with healthy tissues and cells, respectively. Moreover, high expression of lncRNA‑ATB was significantly associated with advanced TNM stage and metastasis in CRC. In addition, the results indicated that lncRNA‑ATB expression predicted the prognosis and overall survival of patients with CRC. Compared with small interfering RNA‑negative control, lncRNA‑ATB knockdown inhibited CRC cell proliferation, migration and invasion, whereas, compared with vector, lncRNA‑ATB overexpression promoted CRC cell proliferation, migration and invasion. Furthermore, the in vivo experiment suggested that lncRNA‑ATB knockdown inhibited tumor growth. The results also indicated that lncRNA‑ATB may contribute to CRC progression via binding to tumor suppressor microRNA‑141‑3p. Collectively, the present study suggested a crucial role of lncRNA‑ATB in CRC tumorigenesis, suggesting that lncRNA‑ATB may serve as an important marker for the diagnosis and development of CRC.