MicroRNA-384 inhibits proliferation migration and invasion of glioma by targeting at CDC42

Gu, G; Wang, Li; Zhang, Junchen; Wang, Hao; Tan, Tan; Zhang, Guang‐Ning

doi:10.2147/ott.s166747

Cited by 16 publications

(18 citation statements)

References 29 publications

(27 reference statements)

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“…Previous studies suggested that miRNAs act by regulating downstream tumor-associated genes. 8–13 It is therefore necessary to investigate the targets of miR-384 in GC to determine the mechanisms underlying its role in the progression of GC. Using mechanistic assays (luciferase reporter assay and western blot), we demonstrated that MTDH was a direct target of miR-384.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of miR-384 has been reported to be downregulated in multiple human cancers, including breast cancer, osteosarcoma, glioma, and non-small-cell lung cancer, 10–13 indicating a tumor suppressive role in these cancers. 10–13 These studies also identified multiple target genes of miR-384, thus establishing its importance in cancers. 10–13 However, the role of miR-384 in GC has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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RETRACTION: miR-384 targets metadherin gene to suppress growth, migration, and invasion of gastric cancer cells

Wang

2019

J Int Med Res

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Objective MicroRNA-384 (miR-384) has been reported to function as a tumor suppressor in multiple cancers; however, its role in gastric cancer (GC) remains unclear. Methods We measured expression levels of miR-384 in GC cell lines and in a normal gastric cell line (GES-1). The association between miR-384 and the metadherin gene ( MTDH) was assessed by luciferase reporter assay and western blot. The effects of the miR-384/MTDH axis on GC cell behaviors were measured by CCK-8, wound-healing, and transwell invasion assays. Results miR-384 was significantly downregulated in GC cell lines compared with normal gastric cells. MTDH was identified as a direct target of miR-384 by bioinformatics analysis, luciferase assay, and western blot. Functional assays demonstrated that miR-384 inhibited GC cell proliferation, migration, and invasion through targeting MTDH. Conclusion These results reveal that miR-384 acts as a tumor suppressor in GC and suggest that the miR-384/MTDH axis may be a potential therapeutic target for GC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTION: miR-384 targets metadherin gene to suppress growth, migration, and invasion of gastric cancer cells

Wang

2019

J Int Med Res

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“…As a chemokine that mediates tumors, CDC42 can participate in the migration and invasion of various cancer cells [33]. Previous research reported that microRNA-384 inhibits proliferation, migration and invasion of glioma by targeting at CDC42 [34]. Yang et al [35] confirmed that downregulation of miR-25 markedly inhibited A549 cell proliferation, induced G1 cell cycle arrest, by targeting CDC42.…”

Section: Discussionmentioning

confidence: 97%

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

Wang

Xie

et al. 2021

Anim Biosci

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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.

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“…Therefore, effective diagnostic and therapeutic strategies for glioma are urgently needed. Recently, studies have confirmed that miRNAs play important roles in tumorigenesis and development, and are involved in the regulation of tumor growth, apoptosis, differentiation, invasion, angiogenesis, and metastasis (15,16). In addition, miRNAs can also act as an oncogenes or tumor-suppressor genes, and their role in the development of gliomas acts on the mechanisms of glioma (17).…”

Section: Discussionmentioning

confidence: 99%

miR‑342 inhibits glioma cell proliferation by targeting GPRC5A

et al. 2019

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accumulating evidence suggests that micrornas (mirnas) play a key role in the biological behaviors and progression of glioma. However, the function and bio-molecular mechanisms of mir-342 in glioma remain largely unclear. in the present study, reverse transcription quantitative-polymerase chain reaction and western blotting were performed to determine the mrna and protein expression levels of the factors investigated. MTT assay was performed to examine the proliferation rates. luciferase reporter assay was performed to test the binding between mirna-342 and its putative target. data indicated that mir-342 expression was markedly decreased in human glioma tissues and cell line u87, and reduced mir-342 expression significantly promoted cell proliferation. In order to explore the mechanisms, G-protein coupled receptor family C group 5 member A (GPRC5A) was identified as a target of mir-342 and depletion of GPrc5a suppressed cell proliferation. Our findings demonstrated that miR-342 regulates the cell proliferation of glioma by targeting GPrc5a, which indicates that mir-342 is a target of interest regarding the treatment of refractory glioma, and it may provide a promising prognostic and therapeutic strategy for glioma treatment.

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MicroRNA-384 inhibits proliferation migration and invasion of glioma by targeting at CDC42

Cited by 16 publications

References 29 publications

RETRACTION: miR-384 targets metadherin gene to suppress growth, migration, and invasion of gastric cancer cells

RETRACTION: miR-384 targets metadherin gene to suppress growth, migration, and invasion of gastric cancer cells

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

miR‑342 inhibits glioma cell proliferation by targeting GPRC5A

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