Abstract
The aim of this study was to investigate the function of microRNA (miR)-193-3p in human intrahepatic cholangiocarcinoma (ICC) tissues and cells. To evaluate whether miR-193-3p was aberrantly upregulated, we used reverse transcription-quantitative polymerase chain reaction to detect the level of miR-193-3p in ICC tissues and ICC-9810 cells. The effects of miR-193-3p downregulation on ICC cell proliferation, migration and invasion were also measured by MTT, wound-healing and Transwell assays. Additionally, transforming growth factor-β receptor type 3 (TGFBR3) was investigated as a direct target of miR-193-3p by dual-luciferase reporter assays and western blot analyses. The results demonstrated that miR-193-3p was aberrantly upregulated in ICC tissues and cell lines. Furthermore, TGFBR3 was confirmed to be a target of miR-193-3p in ICC and was notably upregulated by miR-193-3p knockdown in the ICC-9810 cells. The knockdown of miR-193-3p also exerted direct inhibitory effects on the proliferation, migration and invasion of the ICC-9810 cells. Therefore, we present evidence that miR-193-3p plays a key role in promoting human ICC by regulating TGFBR3.
Highlights
Intrahepatic cholangiocarcinoma (ICC) represents the second most common primary hepatic malignancy, accounting for 5‐10% of liver cancers [1]
The results of reverse transcription‐quantitative poly‐ merase chain reaction (RT‐qPCR) showed that miR‐193‐3p was significantly upregulated in the ICC‐9810 cells when compared with the human intrahepatic biliary epithelial cell (HIBEC) cells (P < 0.01; Fig. 2A)
A previous study suggested that miR‐193‐3p predominantly group. (B) Transwell assay results demonstrated the effects of ICC‐9810 cells invasion. (C) The result showed that miR‐193‐3p suppressed cell migration. (D) The data indicated that miR-193-3p could promote cell invasion. **P
Summary
Intrahepatic cholangiocarcinoma (ICC) represents the second most common primary hepatic malignancy, accounting for 5‐10% of liver cancers [1]. TGFBR3 has been reported to suppresse breast cancer progression by inhibiting cell migration and invasion, as well as angiogenesis. Loss or reduced levels of TGFBR3 expression have been identified in many types of human cancer, including non‐small cell lung cancer (NSCLC), ovarian, prostate, pancreatic, breast and renal cell carcinoma, and overexpression of TGFBR3 can lead to inhibited cancer cell migration and invasion. Gatza et al [11] reported that TGFBR3 was markedly upregulated in human colon cancer and may advance the development of colon cancer to a certain degree. These findings indicated that TGFBR3 might play a dual role in the formation of tumors
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