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Abstract
Accumulating evidences indicate that non-coding RNAs play crucial roles in the progression of an extensive range of carcinomas. This study aimed to investigate the action mechanism of miR-144-5p and miR-451a in cholangiocarcinoma. We found that miR-144-5p and miR-451a were significantly decreased in cholangiocarcinoma patient samples compared to the adjacent normal bile duct samples. The downregulation of these two miRNAs was correlated with a more advanced disease state of cholangiocarcinoma patients. Overexpression of miR-144-5p and miR-451a suppressed the proliferation, invasion and migration of cholangiocarcinoma cells in vitro and inhibited xenograft tumor growth. Knockdown of these two miRNAs had the opposite effects. miR-144-5p and miR-451a regulated the expression of ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 (ST8SIA4), and presented a correlation with ST8SIA4 in patient samples. Overexpression of ST8SIA4 promoted the proliferation, invasion and migration of cholangiocarcinoma cells, and the changes were reversed by upregulating the expression of miR-144-5p and miR-451a. Our findings indicated that miR-144-5p and miR-451a displayed a tumor suppressor role through decreasing the expression of ST8SIA4 in cholangiocarcinoma.
Highlights
Cholangiocarcinoma is a highly aggressive malignancy originating from the epithelial cells of the intra- and extrahepatic biliary ducts [1,2,3]
We demonstrated that miR-144-5p and miR-451a were downregulated in cholangiocarcinoma patient samples. miR-144-5p and miR-451a overexpression inhibited proliferation, invasion and migration of cholangiocarcinoma cells by down-regulating ST8SIA4
We used quantitative RT-PCR to identify the expression of miR144-5p and miR-451a in 23 paired cholangiocarcinoma tissues and adjacent normal tissues. miR-144-5p and miR-451a levels were downregulated in cholangiocarcinoma tissues compared with normal tissues (Figures 1A, B)
Summary
Cholangiocarcinoma is a highly aggressive malignancy originating from the epithelial cells of the intra- and extrahepatic biliary ducts [1,2,3]. The only treatment for cholangiocarcinoma is surgical resection of the tumor, and traditional chemotherapy and radiotherapy have little effect on improving the long-term survival of patients [5]. Therapeutic surgery is only available for early-, but not for advanced-stage patients and the 5-year survival rates of patients is still below miR-144-5p and miR-451a Prevent CCA Growth. Targeted therapy displays obvious advantage of controlling cancer cell proliferation, as well as preventing or delaying recurrence and metastasis [7]. It has a wide range of applications with less adverse effects and can be highly targeted. It is an urgent need to improve our understanding about the molecular pathogenesis of cholangiocarcinoma, which forms a basis for discovering diagnostic markers and new therapeutic targets
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