scholarly journals MicroRNA-224 Promotes Cell Migration and Invasion by Targeting HOXA5 Expression in Hepatocellular Carcinoma

2021 ◽  
Author(s):  
Yuwu Liu ◽  
Chen Lin ◽  
Dongmei Wang ◽  
Sailan Wen ◽  
Junpu Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Migration ◽  
Liver Cancer ◽  
Real Time ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Regulatory Relationship ◽  
Cell Migration And Invasion ◽  
Cell Percentage

Abstract Background MicroRNAs(miRNAs) are involved in the regulation of multiple cellular pathways and play a key role in the development and progression of tumor. Multiple studies have shown that abnormal expression of miRNAs has close relation with the incidence of HCC, but the mechanism of miRNAs in HCC still needs further research. Here, we investigated the mechanism of miR-224 in the invasion and metastasis of liver cancer. Methods We employed real-time quantitative PCR to detect the expression of miR-224 and ADAM17 and HOXA5 in HCC tissues. The expression level of HOXA5 in liver cancer tissues was further verified by immunohistochemistry (IHC). Real time PCR and Western bloting were used to detect the expression changes of ADAM17 and HOXA5 caused by overexpression or silencing of miR-224.Dual luciferase reporter assays demonstrated a direct association between miR-224 and its target gene ADAM17 and HOXA5. The migration and invasion experiment, MTT assay and flow cytometry were performed to investigate the changes of the biology function of HCC cell after overexpression or silencing of miR-224. Results The data showed that miR-224 and ADAM17 were significantly up-regulated and HOXA5 was significantly down-regulated in HCC tissues. The targeted regulatory relationship between miR-224 and its target genes ADAM17 and HOXA5 was also demonstrated. More importantly, we found that miR-224 positively regulates cell migration and invasion in HCC, miR-224 overexpression can promote the migration and invasion of BEL-7402 cell, and miR-224 silencing can suppress the migration and invasion of BEL-7402 cell. MiR-224 overexpression can result in the redistribution of cell cycle, the cell percentage of S phase was increased significantly, the cell percentage of G1 phase was decreased significantly, and there is no noticeable change for the cell percentage of G2 phase. Conclusions These results demonstrated that miR-224 may be exert the function of oncogenes in a particular link of cancer cell growth, it will become a promising biological target in the treatment strategy of hepatocellular carcinoma (HCC).

scholarly journals MicroRNA-224 Promotes Cell Migration and Invasion by Targeting HOXA5 expression in Hepatocellular Carcinoma

2020 ◽  
Author(s):  
Yuwu Liu ◽  
Chen Lin ◽  
Dongmei Wang ◽  
Sailan Wen ◽  
Junpu Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Migration ◽  
Protein Expression ◽  
Close Relation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Growth ◽  
Cell Migration And Invasion ◽  
Cell Percentage ◽  
Biological Target

AbstractMicroRNAs (miRNAs) are involved in the regulation of multiple cellular pathways and play a key role in the development and progression of tumor. Based on the cellular function of their targets, miRNAs play the role of oncogenes or tumor suppressor genes. Multiple studies have shown that abnormal expression of miRNAs has close relation with the incidence of HCC, but the mechanism of miRNAs in HCC still needs further research. In the present study, we showed that the overexpression of miR-224 can reduce the mRNA and protein expression of ADAM17 and HOXA5, the silencing of miR-224 can increase the protein expression of ADAM17 and HOXA5. Dual luciferase reporter assays showed that miR-224 can directly regulate the expression of ADAM17 and HOXA5. Importantly, we found that miR-224 positively regulates cell migration and invasion in HCC, miR-224 overexpression can promote the migration and invasion of BEL-7402 cell, and miR-224 silencing can suppress the migration and invasion of BEL-7402 cell. miR-224 overexpression can result in the redistribution of cell cycle, the cell percentage of S phase was increased significantly, the cell percentage of G1 phase was decreased significantly, and there is no noticeable change for the cell percentage of G2 phase. These results demonstrated that it may be exert the function of oncogenes in a particular link of cancer cell growth. In conclusion, these results suggest that miR-224 will become a promising biological target in the treatment strategy of hepatocellular carcinoma (HCC).

scholarly journals MyoD1 suppresses cell migration and invasion by inhibiting FUT4 transcription in human gastric cancer cells

2019 ◽  
Vol 27 (10-11) ◽  
pp. 773-784 ◽  
Author(s):  
Fei Wu ◽  
Yannan Qin ◽  
Qiuyu Jiang ◽  
Jinyuan Zhang ◽  
Fang Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Target Genes ◽  
Myogenic Differentiation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion ◽  
Chip Sequencing

AbstractMyogenic differentiation 1 (MyoD1) is a transcription factor that promotes expression of muscle-specific genes. MyoD1 is expressed at significantly lower levels in gastric cancer (GC) tissues and cells, and it induces apoptosis in GC cells. However, functions for MyoD1 in GC cell migration and gene expression have not been documented. We show that knockdown of MyoD1 promoted migration and invasion of GC cells, whereas MyoD1 overexpression suppressed migration and invasion. We performed chromatin immunoprecipitation (ChIP)-sequencing to identify MyoD1 target genes in MKN-45 cells. The 2-kb upstream regions (Up2k) of the transcription start sites of 57 genes were probably bound by MyoD1. Six of these genes function in signaling pathways such as synthesis of glycosphingolipid biosynthesis—lacto and neolacto series. MyoD1 inhibited transcription of fucosyltransferase IV (FUT4) by binding directly to the FUT4 F3; this finding was validated by ChIP-quantitative PCR and a luciferase reporter assay. Ulex europaeus agglutinin I, which binds Fucα1-2Galβ1-4GlcNAc, and Lewis antigens showed decreased binding to the plasma membrane of cells that overexpressed MyoD1. Knockdown of FUT4 mimicked MyoD1 overexpression by suppressing GC cell migration and invasion; this result implied that MyoD1 suppressed cell migration and invasion via inhibiting the FUT4/matrix metallopeptidase signaling pathway. In summary, this study demonstrated that MyoD1 suppresses migration and invasion of GC cells by directly binding to the F3 region in the FUT4 Up2k and inhibiting FUT4/type II Lewis antigen expression.

scholarly journals CEP55 Promotes Cell Motility via JAK2–STAT3–MMPs Cascade in Hepatocellular Carcinoma

Cells ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 99 ◽  
Author(s):  
Minjing Li ◽  
Ju Gao ◽  
Defang Li ◽  
Yancun Yin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Migration ◽  
Cell Motility ◽  
Poor Prognosis ◽  
Target Genes ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Stat3 Signaling ◽  
The Poor ◽  
Stimulation Of

Hepatocellular carcinoma (HCC) is one of the most common malignancies and has a poor prognosis. Novel diagnostic or prognostic biomarkers and potential therapeutic targets for HCC are thus urgently needed. CEP55 plays a crucial role in regulating physical cytokinesis. Whether, and how, CEP55 contributes to HCC development remains unclear. Herein, we demonstrate that CEP55 is abnormally upregulated in HCC tissue, and these high levels of CEP55 are closely related to the poor prognosis of HCC patients. Knockdown of CEP55 expression significantly inhibits HCC cell migration and invasion. We also demonstrate that CEP55 physiologically interacts with JAK2 and promotes its phosphorylation; thus, it is a novel regulator of JAK2–STAT3 signaling and its target genes MMP2/9. Finally, blocking JAK2 or STAT3 blunts the stimulation of migration and invasion due to CEP55 overexpression. In summary, our results suggest that CEP55, as an oncogene, promotes HCC cell migration and invasion through regulating JAK2–STAT3–MMPs signaling.

scholarly journals Long non-coding RNA CCDC183-AS1 acts AS a miR-589-5p sponge to promote the progression of hepatocellular carcinoma through regulating SKP1 expression

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
He Zhu ◽  
Hongwei Zhang ◽  
Youliang Pei ◽  
Zhibin Liao ◽  
Furong Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Human Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Regulatory Relationship

Abstract Background Hepatocellular carcinoma (HCC) is a common type of malignant human cancer with high morbidity and poor prognosis, causing numerous deaths per year worldwide. Growing evidence has been demonstrated that long non-coding RNAs (lncRNAs) are closely associated with hepatocarcinogenesis and metastasis. However, the roles, functions, and working mechanisms of most lncRNAs in HCC remain poorly defined. Methods Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of CCDC183-AS1 in HCC tissues and cell lines. Cell proliferation, migration and invasion ability were evaluated by CCK-8 and transwell assay, respectively. Animal experiments were used to explore the role of CCDC183-AS1 and miR-589-5p in vivo. Bioinformatic analysis, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to confirm the regulatory relationship between CCDC183-AS1, miR-589-5p and SKP1. Results Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate. Functionally, overexpression of CCDC183-AS1 markedly promoted HCC cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo, whereas the downregulation of CCDC183-AS1 exerted opposite effects. MiR-589-5p inhibitor counteracted the proliferation, migration and invasion inhibitory effects induced by CCDC183-AS1 silencing. Mechanistically, CCDC183-AS1 acted as a ceRNA through sponging miR-589-5p to offset its inhibitory effect on the target gene SKP1, then promoted the tumorigenesis of HCC. Conclusions CCDC183-AS1 functions as an oncogene to promote HCC progression through the CCDC183-AS1/miR-589-5p/SKP1 axis. Our study provided a novel potential therapeutic target for HCC patients.

scholarly journals CDX2 and Reg IV expression and correlation in gastric cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dandan Chai ◽  
Huifen Du ◽  
Kesheng Li ◽  
Xueliang Zhang ◽  
Xiaoqin Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Real Time ◽  
Real Time Pcr ◽  
Ectopic Expression ◽  
Rank Correlation ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion

Abstract Background Ectopic expression of CDX2 is associated with the development and progression of gastric cancer. Previous studies showed that CDX2 may be an upstream regulator of Reg IV expression in gastric cancer, and our previous report showed that Reg IV upregulated SOX9 expression and enhanced cell migration and invasion in gastric cancer cells. However, the regulatory roles of CDX2 have not been clarified in gastric cancer, and the correlation between CDX2 and Reg IV requires further study. Methods CDX2 and Reg IV were examined in gastric cancer specimens and paired adjacent tissues via real-time PCR and immunohistochemistry (IHC). The association between CDX2 and Reg IV was assessed using the χ2-test and Spearman’s rank correlation. To verify their relationship, knockdown and exogenous expression of CDX2 or Reg IV were performed in AGS and MKN-45 gastric cancer cells, and their expression was subsequently analyzed via a real-time PCR and western blotting. Wound-healing and Transwell assays were used to examine migration and invasion in AGS and MKN-45 cells following CDX2 silencing or overexpression. Results A positive correlation was observed between CDX2 and Reg IV expression at the mRNA and protein levels in gastric cancer tissues. CDX2 silencing significantly downregulated Reg IV expression, and CDX2 overexpression significantly upregulated Reg IV expression in AGS and MKN-45 cells. Neither Reg IV silencing nor overexpression had any effect on CDX2 protein expression in AGS or MKN-45 cells, even though both affected the expression of CDX2 mRNA. Functionally, CDX2 silencing significantly inhibited cell migration and invasion, and CDX2 overexpression significantly promoted cell migration and invasion in AGS and MKN-45 cells. Conclusions Our findings demonstrate that CDX2 expression was positively correlated with that of Reg IV in gastric cancer, and CDX2 promoted cell migration and invasion through upregulation of Reg IV expression in AGS and MKN-45 cells.

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