Bensong Duan

LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma

Numerous studies indicate that long noncoding RNAs (lncRNAs) are dysregulated in hepatocellular carcinoma (HCC) and might serve as potential diagnostic biomarkers and therapeutic targets of HCC. Therefore, it is interesting to globally identify the lncRNAs altered in HCC. In our study, we used microarray to profile the levels of lncRNAs and mRNAs in three pairs of HCC and their adjacent noncancerous samples. We found lncRNA-SVUGP2, which is a splice variant of the UGP2 gene, was down-regulated in HCC samples and correlates with a better prognosis in patients with HCC. Overexpression of lncRNA-SVUGP2 in HepG2 and Hep3B liver cancer cells suppresses cell proliferation in vitro and tumor growth in vivo. Moreover, lncRNA-SVUGP2 suppresses the invasion ability of liver cancer cell lines and downregulates the mRNA and protein levels of MMP2 and 9. Additionally, lncRNA-SVUGP2 positively or negatively correlates with many mRNAs in liver cancer tissues, indicating it is multifunctional in regulating carcinogenesis.Numerous studies indicate that long noncoding RNAs (lncRNAs) are dysregulated in hepatocellular carcinoma (HCC) and might serve as potential diagnostic biomarkers and therapeutic targets of HCC. Therefore, it is interesting to globally identify the lncRNAs altered in HCC. In our study, we used microarray to profile the levels of lncRNAs and mRNAs in three pairs of HCC and their adjacent noncancerous samples. We found lncRNA-SVUGP2, which is a splice variant of the UGP2 gene, was down-regulated in HCC samples and correlates with a better prognosis in patients with HCC. Overexpression of lncRNA-SVUGP2 in HepG2 and Hep3B liver cancer cells suppresses cell proliferation in vitro and tumor growth in vivo. Moreover, lncRNA-SVUGP2 suppresses the invasion ability of liver cancer cell lines and downregulates the mRNA and protein levels of MMP2 and 9. Additionally, lncRNA-SVUGP2 positively or negatively correlates with many mRNAs in liver cancer tissues, indicating it is multifunctional in regulating carcinogenesis.

Decreased expression of miR-193a-3p is associated with poor prognosis in colorectal cancer

Epithelial-mesenchymal transition (EMT) is an early and key process in the metastatic cascade during the progression of colorectal cancer (CRC). The aim of the present study was to identify deregulated EMT-related microRNAs (miRNAs/miRs) of CRC and assess the effect of differentially expressed miRNAs on the prognosis of patients with CRC. Genome-wide expression profiling of miRNAs was assessed in 3 EMT-negative and 3 EMT-positive CRC tissues. Differentially expressed miRNA was further validated in 90 pairs of CRC and corresponding paracarcinoma tissues using the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A total of 6 miRNAs (miR-10a-5p miR-204-3p, miR-1224-3p, miR-193a-3p, miR-365a-3p and miR-3678-3p) were identified to be differentially expressed between different EMT statuses of CRC tissues. Following validation using RT-qPCR, 3 miRNAs (miR-10a-5p, miR-365a-3p and miR-193a-3p) were selected for subsequent studies. The expression levels of miR-10a-5p, miR-193a-3p and miR-365a-3p were markedly increased compared with levels in corresponding paracarcinoma tissues. Survival analyses revealed that down-regulation of miR-193a-3p was associated with worse prognosis of patients with CRC, particularly in female and older patients. The results of the present study indicate that miR-193a-3p may be an EMT-related biomarker and serve as a novel prognostic factor for CRC.

miRNA-338-3p/CDK4 signaling pathway suppressed hepatic stellate cell activation and proliferation

BackgroundActivated hepatic stellate cell (HSC) is the main fibrogenic cell type in the injured liver. miRNA plays an important role in activation and proliferation of HSC.MethodsOur previous study examined the expression profiles of microRNAs in quiescent and activated HSC. Real-time PCR and western blot were used to detect the expression of Collagen type I (Col 1) and Alpha-Smooth Muscle Actin (α-SMA). CCK-8 and Edu assay was used to measure the proliferation rate of HSC. Luciferase reporter gene assay was used to tested the binding between miR-338-3p and Cyclin-dependent kinase 4 (CDK4).ResultsWe found overexpression of miR-338-3p could inhibit Col 1 and α-SMA, two major HSC activation markers, whereas miR-338-3p inhibitor could promote them. Besides, miR-338-3p overexpression could suppress the growth rate of HSC. Further, we found that CDK4, a pleiotropic signaling protein, was a direct target gene of miR-338-3p. Moreover, we found that overexpression of CDK4 could block the effects of miR-338-3p.ConclusionsWe found miR-338-3p is an anti-fibrotic miRNA which inhibits cell activation and proliferation. Our findings suggest that miR-338-3p/CDK4 signaling pathway participates in the regulation of HSC activation and growth and may act as a novel target for further anti-fibrotic therapy.

Correction: LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma

[This corrects the article DOI: 10.18632/oncotarget.18279.].