Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122 | Zendy

Ou Li | Zendy; Weimin Yi | Zendy; Pingzhou Yang | Zendy; Chao Guo | Zendy; Chuang Peng | Zendy

Open Access

Long non‑coding RNA UCA1 promotes proliferation and invasion of intrahepatic cholangiocarcinoma cells through targeting microRNA‑122

Author(s) -

Ou Li,

Weimin Yi,

Pingzhou Yang,

Chao Guo,

Chuang Peng

Publication year - 2019

Publication title -

experimental and therapeutic medicine

Language(s) - English

Resource type - Journals

eISSN - 1792-1015

pISSN - 1792-0981

DOI - 10.3892/etm.2019.7564

Subject(s) - oncogene , gene knockdown , cancer research , ectopic expression , cell growth , microrna , intrahepatic cholangiocarcinoma , long non coding rna , molecular medicine , metastasis , cell , biology , malignancy , cell cycle , cell culture , downregulation and upregulation , pathology , medicine , cancer , gene , biochemistry , genetics

Long non-coding RNA urothelial carcinoma-associated 1 (UCA1) has a role in various common types of human malignancy, including cholangiocarcinoma; however, the expression and function of UCA1 in intrahepatic cholangiocarcinoma (ICC) has remained elusive. In the present study, it was observed that UCA1 expression was significantly upregulated in ICC tissues and cell lines compared with that in the adjacent non-tumour tissues and a human intrahepatic biliary epithelial cell line, respectively. The increased expression of UCA1 was significantly associated with lymph node metastasis and clinical T-stage in ICC. Furthermore, the ICC patients with high expression of UCA1 had a shorter survival time when compared with that of patients with low UCA1 expression. Knockdown of UCA1 caused a significant decrease in ICC cell proliferation and invasion, while ectopic overexpression of UCA1 significantly promoted the proliferation and invasion of ICC cells. Furthermore, it was revealed that UCA1 directly binds to microRNA (miR)-122 to negatively regulate its expression in ICC cells. In addition, miR-122 mimics abrogated the promoting effects of UCA1 on ICC cell proliferation and invasion. In addition, an inverse correlation between miR-122 and UCA1 expression in ICC tissues was observed. In conclusion, the present study demonstrates that the lncRNA UCA1 promotes ICC cell proliferation and invasion at least in part by targeting miR-122, suggesting that the UCA1/miR-122 interaction may become a potential therapeutic target for the treatment of ICC.

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