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Oncogenic role of microRNA‑20a in human uveal melanoma.

Zhou J, Jiang J, Wang S, Xia X - Mol Med Rep (2016)

Bottom Line: The expression levels of miR‑20a were significantly increased in the UM cells and tissues (P<0.05).By contrast, miR‑20a inhibition markedly suppressed the viability and motility of UM cells in vitro.These data provided convincing evidence that miR‑20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China.

ABSTRACT
As a member of the microRNA (miR)-17-92 cluster, miR‑20a has been indicated to be involved in the regulation of the proliferation and invasion of various cancer cells. Previous studies have observed elevated plasma levels of miR‑20a in patients with uveal melanoma (UM), compared with normal controls. In the present study, the potential function of miR‑20a in UM was investigated. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to detect the expression levels of miR‑20a in UM cells and tissues. The functions of miR‑20a on cell proliferation, migration and invasion were determined in vitro using 3‑(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays, respectively. The expression levels of miR‑20a were significantly increased in the UM cells and tissues (P<0.05). Subsequently, miR‑20a mimics were transfected into UM cells, which led to increases in cell growth, migration and invasion activities. By contrast, miR‑20a inhibition markedly suppressed the viability and motility of UM cells in vitro. These data provided convincing evidence that miR‑20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM.

No MeSH data available.


Related in: MedlinePlus

Upregulation of miR-20a promotes UM cell proliferation. The expression levels of miR-20a were significantly elevated in the (A) MUM-2B and (B) MUM-2C cells transfected with miR-20a mimics, but were effectively reduced following transfection with miR-20a inhibitor. In the cell proliferation assay, growth rates were suppressed in the (C) MUM-2B and (D) MUM-2C cells following transfection with miR-20a mimics, with inhibitory efficiencies were 40.38 and 39.66%, respectively. By contrast, the miR-20a inhibitor promoted MUM-2B and MUM-2C cell proliferation. Data are presented as the mean ± standard deviation. UM, uveal melanoma; miR, microRNA; Con, control; OD, optical density.
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f2-mmr-14-02-1560: Upregulation of miR-20a promotes UM cell proliferation. The expression levels of miR-20a were significantly elevated in the (A) MUM-2B and (B) MUM-2C cells transfected with miR-20a mimics, but were effectively reduced following transfection with miR-20a inhibitor. In the cell proliferation assay, growth rates were suppressed in the (C) MUM-2B and (D) MUM-2C cells following transfection with miR-20a mimics, with inhibitory efficiencies were 40.38 and 39.66%, respectively. By contrast, the miR-20a inhibitor promoted MUM-2B and MUM-2C cell proliferation. Data are presented as the mean ± standard deviation. UM, uveal melanoma; miR, microRNA; Con, control; OD, optical density.

Mentions: To investigate whether the upregulation of miR-20a is important in UM cell proliferation, the MUM-2B and MUM-2C cells were transfected with miR-20a mimics or miR-20a inhibitor. As shown in Fig. 2A and B, the expression levels of miR-20a were significantly elevated in the MUM-2B and MUM-2C cells transfected with miR-20a mimics, but was effectively reduced following transfection with the miR-20a inhibitor. In the cell proliferation assay, the growth rate was increased in the MUM-2B and MUM-2C cells following transfection with miR-20a mimics, with promotion efficiencies of 40.38 and 39.66%, respectively (Fig. 2C and D). By contrast, the miR-20a inhibitor suppressed MUM-2B and MUM-2C cell proliferation (Fig. 2C and D).


Oncogenic role of microRNA‑20a in human uveal melanoma.

Zhou J, Jiang J, Wang S, Xia X - Mol Med Rep (2016)

Upregulation of miR-20a promotes UM cell proliferation. The expression levels of miR-20a were significantly elevated in the (A) MUM-2B and (B) MUM-2C cells transfected with miR-20a mimics, but were effectively reduced following transfection with miR-20a inhibitor. In the cell proliferation assay, growth rates were suppressed in the (C) MUM-2B and (D) MUM-2C cells following transfection with miR-20a mimics, with inhibitory efficiencies were 40.38 and 39.66%, respectively. By contrast, the miR-20a inhibitor promoted MUM-2B and MUM-2C cell proliferation. Data are presented as the mean ± standard deviation. UM, uveal melanoma; miR, microRNA; Con, control; OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940053&req=5

f2-mmr-14-02-1560: Upregulation of miR-20a promotes UM cell proliferation. The expression levels of miR-20a were significantly elevated in the (A) MUM-2B and (B) MUM-2C cells transfected with miR-20a mimics, but were effectively reduced following transfection with miR-20a inhibitor. In the cell proliferation assay, growth rates were suppressed in the (C) MUM-2B and (D) MUM-2C cells following transfection with miR-20a mimics, with inhibitory efficiencies were 40.38 and 39.66%, respectively. By contrast, the miR-20a inhibitor promoted MUM-2B and MUM-2C cell proliferation. Data are presented as the mean ± standard deviation. UM, uveal melanoma; miR, microRNA; Con, control; OD, optical density.
Mentions: To investigate whether the upregulation of miR-20a is important in UM cell proliferation, the MUM-2B and MUM-2C cells were transfected with miR-20a mimics or miR-20a inhibitor. As shown in Fig. 2A and B, the expression levels of miR-20a were significantly elevated in the MUM-2B and MUM-2C cells transfected with miR-20a mimics, but was effectively reduced following transfection with the miR-20a inhibitor. In the cell proliferation assay, the growth rate was increased in the MUM-2B and MUM-2C cells following transfection with miR-20a mimics, with promotion efficiencies of 40.38 and 39.66%, respectively (Fig. 2C and D). By contrast, the miR-20a inhibitor suppressed MUM-2B and MUM-2C cell proliferation (Fig. 2C and D).

Bottom Line: The expression levels of miR‑20a were significantly increased in the UM cells and tissues (P<0.05).By contrast, miR‑20a inhibition markedly suppressed the viability and motility of UM cells in vitro.These data provided convincing evidence that miR‑20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China.

ABSTRACT
As a member of the microRNA (miR)-17-92 cluster, miR‑20a has been indicated to be involved in the regulation of the proliferation and invasion of various cancer cells. Previous studies have observed elevated plasma levels of miR‑20a in patients with uveal melanoma (UM), compared with normal controls. In the present study, the potential function of miR‑20a in UM was investigated. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to detect the expression levels of miR‑20a in UM cells and tissues. The functions of miR‑20a on cell proliferation, migration and invasion were determined in vitro using 3‑(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays, respectively. The expression levels of miR‑20a were significantly increased in the UM cells and tissues (P<0.05). Subsequently, miR‑20a mimics were transfected into UM cells, which led to increases in cell growth, migration and invasion activities. By contrast, miR‑20a inhibition markedly suppressed the viability and motility of UM cells in vitro. These data provided convincing evidence that miR‑20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM.

No MeSH data available.


Related in: MedlinePlus