Abstract
Hepatocellular carcinoma (HCC) has threatened the health of humans, and some evidence has indicated that miR-466 involves the progressions of some cancers. This study focused on the role of miR-466 in the formation and development of HCC. The expression levels of miR-466 in the tissues of patients and HCC cell lines were measured by qRT-PCR, and CCK-8, transwell assay, and flow cytometry assay were used to observe the functions of miR-466 on the HCC cells. Moreover, the miRNA databases, dual-luciferase reporter assay, and Western blot were used for the investigation of the regulation mechanism of miR-466 on HCC cells. The results showed that miR-466 was significantly downregulated in HCC tissues and cell lines, and inhibited proliferation, invasion, and high apoptosis were found in HCC cells when miR-466 was overexpressed. The results confirmed that FMNL2 was a target of miR-466, and increased FMNL2 could reverse the effects of miR-466 on the phenotype of HCC cells. Besides, it was also found that miR-466 was involved in the regulation of NF-κB and Wnt/β-catenin pathways in HCC cells via targeting FMNL2. In conclusion, the results of this study suggest that miR-466 regulates the activities of NF-κB and Wnt/β-catenin pathways to inhibit the progression of HCC cells via targeting FMNL2.
Highlights
Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality, and up to 600000 people die from this disease worldwide every year [1, 2]
To observe the connection between miR-466 and hepatocellular carcinoma, the tissues of the patients and normal and tumor cell lines were used to measure the expression level of miR-466. e Quantitative Reverse Transcription PCR (qRT-PCR) showed that the miR-466 was significantly downregulated in the tumor tissues compared with the paracancerous tissues (Figure 1(a), P < 0.01)
To explore the functions of miR-466 in hepatocellular carcinoma cells, the miR-466 mimics were transfected into Huh7, and CCK-8 assay, transwell assay, and flow cytometry assay were used to reflect the changes in proliferation, invasion, and apoptosis levels of the cells. e CCK-8 assay showed that the proliferation of Huh7 transfected with miR-466 mimics was visibly inhibited compared with the cells transfected with miRNA negative control (miR-NC) (Figure 2(a), P < 0.01). e transwell assay reflected that Huh7 cells transfected with miR-466 mimics expressed low invasive abilities compared with the cells transfected with miR-NC (Figure 2(c), P < 0.01)
Summary
Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality, and up to 600000 people die from this disease worldwide every year [1, 2]. Some significant improvements have been achieved in clinical diagnosis and treatment. Erefore, there is an urgent demand to search for novel molecules and provide much more strategies for clinical diagnosis and treatment. Multiple studies have indicated that miRNAs dysfunction plays an important role in the formations and developments of many diseases ranging from cardiovascular deterioration to tumors [11, 12]. Erefore, regulating the expression of some special miRNAs has been proved as a promising diagnostic and therapeutic system for cancer in clinical treatment. Multiple studies have indicated that miRNAs dysfunction plays an important role in the formations and developments of many diseases ranging from cardiovascular deterioration to tumors [11, 12]. erefore, regulating the expression of some special miRNAs has been proved as a promising diagnostic and therapeutic system for cancer in clinical treatment. e
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