Abstract
Our study investigated whether microRNA-122 (miR-122) played important roles in the proliferation, invasion and apoptosis of human cholangiocarcinoma (CC) cells. QBC939 and RBE cells lines were chosen and divided into five groups: miR-122 mimic group, anti-miR-122 group, negative control (NC) group, mock group and blank group. MiR-122 expression was measured by qRT-PCR. Roles of miR-122 in cell proliferation, apoptosis and invasion were investigated using MTT assay, flow cytometer and Transwell invasion assay, respectively. MiR-122 expression was lower in CC tissues and QBC939 cell than that in normal bile duct tissues, HCCC-9810 and RBE cells. In both QBC939 and RBE cells lines, miR-122 expression was higher in miR-122 mimic group than that in NC group, mock group and blank group; opposite results were found in anti-miR-122 group. Cell proliferation and invasion were remarkably inhibited in miR-122 mimic group after 48 h/72 h transfection, while apoptotic cells numbers were much greater in miR-122 mimic group; the opposite results were obtained from anti-miR-122 group (all P < 0.05). MiR-122 expression was significantly weaker in CC tissues, and miR-122 overexpression might play pivotal roles in inhibiting proliferation, stimulating apoptosis and suppressing invasion of CC cells, suggesting a new target for CC diagnosis and treatment.
Highlights
Cholangiocarcinoma (CC) is the second commonest primary liver malignancy after hepatocellular carcinoma (HCC) and is generally classified into three forms including intrahepatic cholangiocarcinoma (ICC), hilar cholangiocarcinoma and extrahepatic cholangiocarcinoma (ECC)[1]
MiR-122 serves as functional miRNA involved in regulating lipid metabolism, cell differentiation, hepatic metabolism and hepatitis C virus replication[22]
The design of the experiment constituted a knockout mouse model modeling the loss of miRNA in hepatocytes, and liver disruptions including steatosis, inflammation and hepatocyte apoptosis were identified, suggesting that miRNAs played a key role in the liver function and that miR-122 may be associated with hepatocarcinogenesis by influencing hepatocyte survival and tumor progression[23,24]
Summary
Cholangiocarcinoma (CC) is the second commonest primary liver malignancy after hepatocellular carcinoma (HCC) and is generally classified into three forms including intrahepatic cholangiocarcinoma (ICC), hilar cholangiocarcinoma and extrahepatic cholangiocarcinoma (ECC)[1]. MiRNAs, the non-coding RNA molecules, act as post-transcription regulators of gene expression by binding to the complementary sequences in the 3′ untranslated region[10]. MicroRNA-122 (miR-122) is the most abundantly expressed miRNA in human liver cells, and it plays an important role in suppressing cell proliferation and controlling cell viability by targeting antiapoptotic B-cell lymphoma 2 (Bcl-2) family protein Bcl-2 and activating caspase-3 (http:// www.scirp.org/journal/PaperInformation.aspx?paperID= 22969). MiR-122 plays a role in various types of cancer by regulating the expressions of the oncogenic proteins such as disintegrin, metalloproteinase domain 10, transcription factor and receptor tyrosine kinase, which are involved in cell adhesion, migration and invasion[13]. The function of miR-122 as tumor suppressor may inhibit the development of CC by binding to target genes related with tumor cell proliferation, apoptosis, invasion and angiogenesis[14]. We investigated the role of miR122 in cell proliferation, apoptosis and invasion in CC
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
