miR-185 inhibits cell migration and invasion of hepatocellular carcinoma through CDC42

Zhang, Qingjun; Chen, Yun; Liu, Ke

doi:10.3892/ol.2018.8971

Cited by 13 publications

(11 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Literature has also recorded that enhanced miR-185 suppressed CRC cancer cell colony formation ability and enhanced apoptosis 29 . A similar study by Zhang et al has reported that miR-185 was downregulated in HCC, and enhancing miR-185 could dampen HCC cell migration and invasion 30 . Anyhow, miR-185 was an-tumor in cancers and its upregulation served to slow down tumor progression.…”

Section: Discussionmentioning

confidence: 58%

RETRACTED ARTICLE: Long noncoding RNA HEIH depletion depresses esophageal carcinoma cell progression by upregulating microRNA-185 and downregulating KLK5

Wang

Hao

et al. 2020

Cell Death Dis

View full text Add to dashboard Cite

Numerous studies have reported the association of long non-coding RNAs (lncRNAs) in cancers, yet the function of lncRNA high expressed in hepatocellular carcinoma (HEIH) in esophageal carcinoma (EC) has seldom been explored. Here, we aimed to explore the mechanism of HEIH on EC via microRNA-185 (miR-185)/kallikrein-related peptidase 5 (KLK5) modulation. Cancer and non-tumoral tissues were collected, in which HEIH, miR-185 and KLK5 expression were detected, as well as their correlations. Also, the relation between the prognosis of EC patients and HEIH/miR-185/KLK5 expression was clarified. EC cells (KYSE-30 and TE-1) were screened for subsequent gain- and loss-of-function assays and their biological functions were further monitored. Tumor volume and weight in EC mice were also measured. Results from this study indicated that HEIH and KLK5 were elevated and miR-185 was declined in EC. The positive correlation was seen in HEIH and KLK5 expression, while the negative correlation was observed in HEIH or KLK5 and miR-185 expression. High HEIH and KLK5 indicated worse prognosis and high miR-185 suggested better prognosis of EC patients. Depleting HEIH or restoring miR-185 suppressed the malignant phenotypes of EC cells, and delayed tumor growth in EC mice. HEIH was found to bind with miR-185 to regulate KLK5 expression. Overexpressing KLK5 alone promoted EC cell progression while up-regulating miR-185 reversed such effects on EC cells. Collectively, we reveal that HEIH depletion dampens EC progression by upregulating miR-185 and downregulating KLK5, which provides novel treatments for EC.

show abstract

Section: Discussionmentioning

confidence: 58%

RETRACTED ARTICLE: Long noncoding RNA HEIH depletion depresses esophageal carcinoma cell progression by upregulating microRNA-185 and downregulating KLK5

Wang

Hao

et al. 2020

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…In this study, three softwares: TargetScan, miRDB and miRanda were used to predict the target genes for Previous research shown that CDC42 is a potential target of miR-185. For example, Zhang et al [21] confirmed that CDC42 is a direct target of miR-185 in human hepatocellular carcinoma using luciferase reporter assays. Liu et al [28] shown that miR-185 expression significantly suppressed the RhoA and CDC42 3'UTR activities using a luciferase-reporter assay, and could inhibit the proliferation and invasion of human colorectal cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous study, we researched the expression profiles of the ileum miRNAs of 7 days piglets infected with Clostridium perfringens type C using small RNA-Seq, and found that ssc-miR-185 was differentially expressed between the resistant groups and susceptibility groups of diarrhea piglets [14]. It is reported that miR-185 can play important roles in a variety of cancers, covering pancreatic cancer [15], bladder cancer [16], non-small cell lung cancer [17], prostate carcinoma [18], gastric cancer [19], breast cancer [20], hepatocellular carcinoma [21] and colorectal cancer [22]. In addition, miR-185 can also play a regulatory role in response the immune inflammatory.…”

Section: Introductionmentioning

confidence: 99%

ssc-miR-185 targets cell division cycle 42 and promotes the proliferation of intestinal porcine epithelial cell

Wang

Xie

et al. 2021

Anim Biosci

View full text Add to dashboard Cite

Objective: microRNAs (miRNAs) can play a role in a variety of physiological and pathological regulation, and its role is achieved by regulating the expression of target genes. Our previous high-throughput sequencing found that ssc-miR-185 plays an important regulatory role in piglet diarrhea, but its specific target genes and functions in intestinal porcine epithelial cell (IPEC-J2) are still unclear. We intended to verify the target relationship between porcine miR-185 and cell division cycle 42 (CDC42) gene in IPEC-J2, and explored the effect of miR-185 on the proliferation of IPEC-J2 cells. Methods: The TargetScan, miRDB and miRanda softwares were used to predict the target genes of porcine miR-185, and CDC42 was selected as a candidate target gene. The CDC42-3'UTR-wild type (WT) and CDC42-3'UTR-mutant type (MUT) segments were successfully cloned into pmirGLO luciferase vector, and the luciferase activity was detected after co-transfection with miR-185 mimics and CDC42-3'UTR. The expression level of CDC42 was analyzed using qPCR and Western blot. The proliferation of IPEC-J2 was detected using CCK-8, MTT and EdU assays. Results: Double enzyme digestion and sequencing confirmed that CDC42-3'UTR-WT and CDC42-3'UTR-MUT were successfully cloned into pmirGLO luciferase reporter vector, and the luciferase activity was significantly reduced after co-transfection with miR-185 mimics and CDC42-3'UTR (WT). Further we found that the mRNA and protein expression level of CDC42 were down-regulated after transfection with miR-185 mimics, while the opposite trend was observed after transfection with miR-185 inhibitor (p < 0.01). In addition, the CCK-8, MTT and EdU results demonstrated that miR-185 promotes IPEC-J2 cells proliferation by targeting CDC42. Conclusion: These findings indicate that porcine miR-185 can directly target CDC42 and promote the proliferation of IPEC-J2 cells. However, the detailed regulatory mechanism of miR-185/CDC42 axis in piglets resistance to diarrhea is yet to be further investigation.

show abstract

“…Two additional targets of miR-185 are the Rho GTPases, CDC42 and RHOA ( Table 4 ), implicated in cell cycle, cellular function and maintenance, and cell signaling. By targeting these mRNAs, miR-185 has been shown to inhibit cell proliferation and migration in hepatic, colorectal, and lung cancer cell models [ 45 , 46 , 47 , 48 ]. Importantly, miR-185 can also interact with and target the long noncoding RNA FOXD2-AS1, known to inhibit cell proliferation, migration, and epithelial–mesenchymal transition (EMT) in glial cells and renal fibrosis models [ 49 , 50 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants

et al. 2021

View full text Add to dashboard Cite

Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in neonates as a consequence of preterm birth, arrested fetal lung development, and inflammation. The incidence of BPD remains on the rise as a result of increasing survival of extremely preterm infants. Severe BPD contributes to significant health care costs and is associated with prolonged hospitalizations, respiratory infections, and neurodevelopmental deficits. In this study, we aimed to detect novel biomarkers of BPD severity. We collected tracheal aspirates (TAs) from preterm babies with mild/moderate (n = 8) and severe (n = 17) BPD, and we profiled the expression of 1048 miRNAs using a PCR array. Associations with biological pathways were determined with the Ingenuity Pathway Analysis (IPA) software. We found 31 miRNAs differentially expressed between the two disease groups (2-fold change, false discovery rate (FDR) < 0.05). Of these, 4 miRNAs displayed significantly higher expression levels, and 27 miRNAs had significantly lower expression levels in the severe BPD group when compared to the mild/moderate BPD group. IPA identified cell signaling and inflammation pathways associated with miRNA signatures. We conclude that TAs of extremely premature infants contain miRNA signatures associated with severe BPD. These may serve as potential biomarkers of disease severity in infants with BPD.

show abstract

miR-185 inhibits cell migration and invasion of hepatocellular carcinoma through CDC42

Cited by 13 publications

References 32 publications

RETRACTED ARTICLE: Long noncoding RNA HEIH depletion depresses esophageal carcinoma cell progression by upregulating microRNA-185 and downregulating KLK5

RETRACTED ARTICLE: Long noncoding RNA HEIH depletion depresses esophageal carcinoma cell progression by upregulating microRNA-185 and downregulating KLK5

ssc-miR-185 targets cell division cycle 42 and promotes the proliferation of intestinal porcine epithelial cell

MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants

Contact Info

Product

Resources

About