MiR-30b-5p modulates glioma cell proliferation by direct targeting MTDH

Zhang, Daobao; Li, Yong; Zheng, Niandong; Wu, Honggang; Zhang, Zhao; Xu, Jianguo

doi:10.1016/j.sjbs.2018.02.015

Cited by 17 publications

(14 citation statements)

References 35 publications

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“…Glioma is regarded as the most common malignant tumor of the human central nervous system, and glioblastoma accounts for about 80% of malignant brain tumors, which is characterized by aggressive angiogenesis. 1 Glioma has high invasion, recurrence, and mortality rate because the glioma cells growth and proliferation has considerably dependence on angiogenesis. Angiogenesis is regulated by the interaction of proangiogenic and antiangiogenic factors.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-503 Inhibits Proliferation, Migration, And Angiogenesis Of Glioma By Acting On VEGFA Through Targeting LRIG2</p>

Sun¹,

Shu²,

Tao³

2019

CMAR

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Background: Glioma is a common malignant tumor of the human central nervous system, and the pathological characteristics include invasive growth, angiogenesis, and so on. Ectopic expression of miR-503 works as a critical factor in cancer cell proliferation, migration, and capillary-like tube formation. The potential mechanisms of miR-503 in angiogenesis of glioma cells are still not reported. Methods: The expression levels of miR-503, LRIG2, and VEGFA mRNA and protein were performed by quantitative reverse transcription-PCR or Western blot assay. Dual-Luciferase reporter gene assay was used to determine the interaction between miR-503 and LRIG2. The concentration of VEGFA was measured using the ELISA method. The cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were analyzed by MTT assay, transwell detection, and tube formation assay, respectively. Results: The expression levels of LRIG2 and VEGFA were reduced in glioma cells with miR-503 overexpression and enhanced with miR-503 inhibition. Moreover, cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were alleviated with miR-503 mimics transfection. VEGFA and miR-503 inhibitor promoted cell proliferation, cell migration, and angiogenesis. Luciferase reporter gene assay revealed that miR-503 could directly target LRIG2. Furthermore, knockdown of LRIG2 or addition of VEGF inhibitor bevacizumab could abrogate the effect of miR-503 inhibitor on VEGFA expression, as well as the promotion of cell proliferation, migration, and angiogenesis. Conclusion: MiR-503 mediated LRIG2 suppression and regulated the expression of VEGFA, thereby reducing cell proliferation, migration, and angiogenesis of glioma cells. These results provide new insight into the action mechanism of miR-503-modulated signaling pathway in angiogenesis of glioma cells.

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Section: Introductionmentioning

confidence: 99%

<p>miR-503 Inhibits Proliferation, Migration, And Angiogenesis Of Glioma By Acting On VEGFA Through Targeting LRIG2</p>

Sun¹,

Shu²,

Tao³

2019

CMAR

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“…MiRNA‐30b has been reported to be involved in the onset and development of various diseases including glioma cancers and hepatocellular carcinoma. MiR‐30b regulated glioma cell proliferation by directly targeting MTDH (Zhang et al, ). In hepatocellular carcinoma, miR‐30b inhibited development of human hepatocellular carcinoma by repressing cell proliferation and cell cycle (Qin, Chen, Wu, & Liu, ).…”

Section: Discussionmentioning

confidence: 99%

miR‐30b protects nigrostriatal dopaminergic neurons from MPP(+)‐induced neurotoxicity via SNCA

et al. 2020

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Objective To explore the function of miR‐30b in pathogenesis of Parkinson's disease (PD) and its underlying molecular mechanism. Materials and Methods We used 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPP(+)) as a tool for constructing the PD cell model, using miR‐30b mimics or inhibitors to manipulate miR‐30b level for an experimental model of acquisition. The cell viability of SH‐SY5Y was detected by CCK, and luciferase was used to screen the binding of target genes. The protein levels of SNCA were measured by Western blot. Then, we investigate the changes in pro‐ and anti‐apoptotic markers with or without miR‐30b treatment. Results There was a significant low expression of MiR‐30b in MPP(+)‐induced cells. SH‐SY5Y cell viability was rescued by MiR‐30b overexpression. Luciferase experiments showed that MiR‐30b may bind to the 3′‐UTR side of SNCA and inhibited its expression. By Western blot, the SNCA level was markedly decreased by miR‐30b. miR‐30b attenuated the upregulation of Bax and the depletion of Bcl‐2 induced by MPP(+).

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“…Approximately 60% of human genes are thought to be regulated by miRNAs, which suggests that miRNAs may be involved in multiple cellular processes (23). Numerous miRNAs have been identified to be critical players in the progression of glioma (9,24,25). For example, miR-30b-5p overexpression significantly inhibited glioma cell proliferation in vitro by downregulating the expression of metadherin (24).…”

Section: Discussionmentioning

confidence: 99%

miR‑490‑3p functions as a tumor suppressor in glioma by inhibiting high‑mobility group AT‑hook 2 expression

Zhang

Wang

et al. 2019

Exp Ther Med

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Glioma is one of the most common types of malignant cancer and the significance of microRNAs (miRNAs) in cancer therapy has been demonstrated. In the current study, miR-490-3p expression was significantly downregulated in glioma tissue and cell lines. Overexpression of miR-490-3p inhibited glioma cell proliferation and migration in vitro . In addition, the high-mobility group AT-hook 2 (HMGA2) was identified as a candidate target gene of miR-490-3p. The current study demonstrated that miR-490-3p mimic could inhibit HMGA2 protein expression in glioma cells. In addition, correlation analysis demonstrated that miR-490-3p and HMGA2 expression was inversely correlated in glioma tissues. Furthermore, the inhibitory effect of miR-490-3p mimic on cell proliferation and migration was partially reversed by the overexpression of HMGA2. Taken together, these results suggest that miR-490-3p may have a tumor suppressive role in glioma and therefore miR-490-3p may be a new target for the treatment of glioma.

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MiR-30b-5p modulates glioma cell proliferation by direct targeting MTDH

Cited by 17 publications

References 35 publications

<p>miR-503 Inhibits Proliferation, Migration, And Angiogenesis Of Glioma By Acting On VEGFA Through Targeting LRIG2</p>

<p>miR-503 Inhibits Proliferation, Migration, And Angiogenesis Of Glioma By Acting On VEGFA Through Targeting LRIG2</p>

miR‐30b protects nigrostriatal dopaminergic neurons from MPP(+)‐induced neurotoxicity via SNCA

miR‑490‑3p functions as a tumor suppressor in glioma by inhibiting high‑mobility group AT‑hook 2 expression

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