scholarly journals MicroRNA-214-5p Inhibits the Invasion and Migration of Hepatocellular Carcinoma Cells by Targeting Wiskott-Aldrich Syndrome Like

2018 ◽  
Vol 46 (2) ◽  
pp. 757-764 ◽  
Author(s):  
Hongdan Li ◽  
Haoqi Wang ◽  
Zhen Ren
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Hepatocellular Carcinoma Cells ◽  
Invasion And Migration ◽  
Wiskott Aldrich Syndrome ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
And Migration

Background/Aims: This study aims to explore the effects of microRNA-214-5p (miR-214-5p) on the invasion and migration of Hepatocellular Carcinoma cells (HCC). Methods: Hepatocellular Carcinoma tissues and adjacent normal tissues from 44 hepatocellular carcinoma patients were prepared for this study. The HepG2 and BEL-7402 cells were transfected with miR-214-5p mimic and inhibitor. qRT-PCR was performed to detect the expressions of miR-214-5p. Transwell assays were used to detect the invasion and migration assays in HepG2 and BEL-7402 cells. A dual-luciferase reporter assay was conducted to examine the effect of miR-214-5p on Wiskott-Aldrich Syndrome Like (WASL/ N-WASP). Western blot and qRT-PCR were used to measure the expressions of the E-cadherin, N-cadherin and Vimentin proteins. Transwell chamber assays were performed to detect cell invasion and migration. Results: Compared with normal tissues, HCC tissues demonstrated significantly lower expression of miR-214-5p. Overexpression of miR-214-5p significantly inhibited the migration and invasion of HCC cells and inhibition of miR-214-5p promoted the migration and invasion. Additionally, miR-214-5p suppressed the epithelial-mesenchymal transition (EMT). Further study showed WASL was a putative target gene of miR-214-5p. Up-regulating the expression of WASL could reverse the inhibition effect of miR-214-5p on invasion and migration. Conclusion: Our data suggested that miR-214-5p inhibited the invasion and migration of HepG2 and BEL-7402 by targeting WASL in Hepatocellular carcinoma.

scholarly journals miR-100 Suppresses the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma Cells via Targeting CXCR7

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yiman Ge ◽  
Jia Shu ◽  
Gang Shi ◽  
Fuguo Yan ◽  
Yejing Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Antitumor Effects ◽  
Hepatocellular Carcinoma Cells ◽  
Invasion And Migration ◽  
Reporter Assays ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Endothelial Growth Factor

This study is to elucidate the functions of miR-100 in hepatocellular carcinoma progression and to explore the underlying mechanisms. Expression levels of miR-100 in normal-cancer hepatocellular carcinoma tissues were measured using quantitative real-time PCR (qRT-PCR). The invasive and proliferative abilities of hepatocellular carcinoma cell lines transfected with mimic-NC or mimic-miR-100 were measured using transwell, CCK-8, and colony formation assays. The binding sites between CXCR7 and miR-100 were determined using luciferase reporter assays. The correlation of CXCR7 and miR-100 in hepatocellular carcinoma progression was further confirmed by cotransfection assays. Our results showed that miR-100 was significantly lower expressed in hepatocellular carcinoma tissues and negatively associated with CXCR7 expression. Cell functional assays’ results found that upregulation of miR-100 inhibited the proliferative, invasive, and migrative abilities in hepatocellular carcinoma cells. Luciferase reporter assay suggested that CXCR7 mRNA and miR-100 bound one another. Increasing CXCR7 expression reversed the inhibitive effects of upregulated miR-100 in hepatocellular carcinoma cells. Further study showed that miR-100/CXCR7 played a role in hepatocellular carcinoma progression by regulating metalloproteinase-2 (MMP2) and vascular endothelial growth factor (VEGF). Conclusively, miR-100 exerts antitumor effects on hepatocellular carcinoma. Overexpression of miR-100 attenuates the invasive and proliferative abilities of hepatocellular carcinoma cells by targeting CXCR7.

Delivery of microRNA-21-sponge and pre-microRNA-122 by MS2 virus-like particles to therapeutically target hepatocellular carcinoma cells

2021 ◽  
pp. 153537022110356
Author(s):  
Jiawei Zhang ◽  
Dandan Li ◽  
Rui Zhang ◽  
Rongxue Peng ◽  
Jinming Li
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Hepatocellular Carcinoma Cells ◽  
Virus Like Particles ◽  
Invasion And Migration ◽  
Mrna Targets ◽  
And Migration ◽  
Microrna Dysregulation ◽  
Hcc Cells

MicroRNAs are related to the development of hepatocellular carcinoma and can serve as potential therapeutic targets. Therapeutic strategies increasing tumor-suppressive microRNAs and reducing oncogenic microRNAs have been developed. Herein, the effects of simultaneously altering two microRNAs using MS2 virus-like particles were studied. The sequences of microRNA-21-sponge and pre-microRNA-122 were connected and cloned into a virus-like particle expression vector. Virus-like particles containing microRNA-21-sponge and pre-microRNA-122 sequences were prepared and crosslinked with a cell-specific peptide targeting hepatocellular carcinoma cells. Delivery effects were studied using RT-qPCR and functional assays to investigate the level of target mRNAs, cell toxicity, and the effects of proliferation, invasion, and migration. Virus-like particles delivered miR-21-sponge into cells, with the Ct value reaching 10 at most. The linked pre-miR-122 was processed into mature miR-122. The mRNA targets of miR-21 were derepressed as predicted and upregulated 1.2–2.8-fold, and the expression of proteins was elevated correspondingly. Proliferation, migration, and invasion of HCC cells were inhibited by miR-21-sponge. Simultaneous delivery of miR-21-sponge and miR-122 further decreased proliferation, migration, and invasion by up to 34%, 63%, and 65%, respectively. And the combination promoted the apoptosis of HCC cells. In conclusion, delivering miR-21-sponge and miR-122 using virus-like particles modified by cell-specific peptides is an effective and convenient strategy to correct microRNA dysregulation in hepatocellular carcinoma cells and is a promising therapeutic strategy for hepatocellular carcinoma.

scholarly journals MiR-92a-3p promote s invasion and migration of hepatocellular carcinoma cells by targeting PTEN

2021 ◽  
Author(s):  
Yilin Hu ◽  
Huiling Sun ◽  
Qiping Lu ◽  
Hongliang Mei ◽  
Rong Liu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mutation Frequency ◽  
Biological Information ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Clinical Samples ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
And Migration ◽  
The Impact

Abstract Background MiR-92a-3p has been reported to play a part in hepatocellular carcinoma (HCC), a leading type of lethal cancer around the world. In this study, we explored the function and mechanism of miR-92a-3p in HCC. Methods Firstly, the expression of miR-92a-3p in HCC along with its relationship with PTEN was analyzed through biological information. To investigate the impact of miR-92a-3p on the migration and invasion of HCC cells, we performed scratch wound healing and transwell assays. Next, RT-qPCR, western blot and dual luciferase reporter gene assays were conducted to determine whether PTEN is targeted by miR-92a-3p, which was then verified through rescue assays. Afterwards, in vivo animal experiments were carried out to determine the function of miR-92a-3p in HCC tissues. As an established fact, PETN is an anti-oncogene with frequent mutation inactivation in human cancers. Thus, we used the database to predict the mutation of PETN and its mutation frequency. Finally, CRISPR-cas12a was applied to detect the R130Q mutation on PETN in HCC clinical samples. Results This study found that the migration and invasion of HCC could be suppressed by inhibiting miR-92a-3p, which regulates the proliferation, migration and invasion of HCC through the regulation of PETN. The bioinformatics analysis indicated higher mutation frequency of R130Q/G/L* site on the PETN gene, and greater impact of R130Q site mutation on the progression of HCC. CRISPR-cas12a detected 26 cases of R130Q mutations on PTEN in 40 HCC clinical samples Conclusion Collectively, this study revealed that miR-92a-3p promoted the invasion and migration of HCC by targeting PTEN, and that the stability of PETN also affected the development of HCC, which may enrich and deepen our knowledge on the progression of HCC.

scholarly journals A long non-coding RNA lncRNA-PE promotes invasion and epithelial–mesenchymal transition in hepatocellular carcinoma through the miR-200a/b-ZEB1 pathway

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770575 ◽  
Author(s):  
Yuan Shen ◽  
Shanshan Liu ◽  
Hanyu Yuan ◽  
Xiaomin Ying ◽  
Hanjiang Fu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Tissue Samples ◽  
Hepatocellular Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Non Coding Rnas ◽  
And Migration

Long non-coding RNAs have been revealed to play important roles in the progression of hepatocellular carcinoma. However, the detailed mechanisms underlying their activities are not fully understood. Using microarray technology, a number of long non-coding RNAs were previously identified to be aberrantly expressed in hepatocellular carcinoma. In this study, one of these long non-coding RNAs, designated lncRNA-PE (lncRNA promotes epithelial–mesenchymal transition), was further explored to study its expression profile and function. A cohort of human hepatocellular carcinoma tissue samples combined with benign controls and established human hepatocellular carcinoma cell lines were examined for the expression of lncRNA-PE. The biological functions of lncRNA-PE were examined by wound-healing and Transwell assays, which revealed that lncRNA-PE promotes cell invasion and migration. By detecting the level of epithelial–mesenchymal transition markers, lncRNA-PE was revealed to promote epithelial–mesenchymal transition in hepatocellular carcinoma cells. Further study suggested that lncRNA-PE downregulated miR-200a/b by repressing the primary transcript expression, enhanced ZEB1 expression, and promoted epithelial–mesenchymal transition of hepatocellular carcinoma cells. All these data imply that lncRNA-PE might play an important role in hepatocellular carcinoma development via the miR-200a/b-ZEB1 pathway.

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