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MicroRNA-19a mediates gastric carcinoma cell proliferation through the activation of nuclear factor-κB.

Yang F, Wang H, Jiang Z, Hu A, Chu L, Sun Y, Han J - Mol Med Rep (2015)

Bottom Line: The present study predominantly focussed on the effects of microRNA (miR)‑19a on NF‑κB activation.The results of the western blot analysis demonstrated that the protein levels of p65 increased when the MGC‑803 cells were transfected with miR‑19a mimics.In addition, the downstream target genes of miR‑19a, including intercellular adhesion molecule, vascular cell adhesion molecule and monocyte chemoattractant protein‑1, were upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Tumor Research and Therapy Center, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.

ABSTRACT
In gastric carcinoma, the nuclear factor‑κB (NF‑κB) signaling pathway is highly active, and the constitutive activation of NF‑κB prompts malignant cell proliferation. MicroRNAs are considered to be important mediators in the regulation of the NF‑κB signaling pathway. The present study predominantly focussed on the effects of microRNA (miR)‑19a on NF‑κB activation. Reverse transcription‑quantitative polymerase chain reaction was used to quantify the relative levels of miR‑19a in gastric carcinoma cells. MTT assays were used to determine the effect of miR‑19a on cellular proliferation. To detect the activation of NF‑κB, western blotting was performed to measure the protein levels of NF‑κB and the products of its downstream target genes. To define the target genes, luciferase reporter assays were used. miR‑19a was found to be markedly upregulated in gastric carcinoma cells. The overexpression of miR‑19a resulted in proliferation and enhanced migratory capabilities of the MGC‑803 gastric carcinoma cell line. The results of the western blot analysis demonstrated that the protein levels of p65 increased when the MGC‑803 cells were transfected with miR‑19a mimics. In addition, the downstream target genes of miR‑19a, including intercellular adhesion molecule, vascular cell adhesion molecule and monocyte chemoattractant protein‑1, were upregulated. The results of the luciferase assay indicated that IκB‑α was the target gene of miR‑19a. Therefore, the results of the present study suggested that miR‑19a enhances malignant gastric cell proliferation by constitutively activating the NF‑κB signaling pathway.

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Expression levels of miR-19a in human gastric carcinoma cells. Reverse transcription-quantitative polymerase chain reaction analysis of the expression of miR-19a in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines and in the immortalized GES-1 gastric epithelial cell line. RNU48 was used as an endogenous control. Data are presented as the mean ± standard error of three independent experiments.*P<0.05, vs. control. miR, microRNA.
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f1-mmr-12-04-5780: Expression levels of miR-19a in human gastric carcinoma cells. Reverse transcription-quantitative polymerase chain reaction analysis of the expression of miR-19a in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines and in the immortalized GES-1 gastric epithelial cell line. RNU48 was used as an endogenous control. Data are presented as the mean ± standard error of three independent experiments.*P<0.05, vs. control. miR, microRNA.

Mentions: The relative levels of miR-19a in human gastric carcinoma cells were detected using RT-qPCR. Compared with the GES-1 immortalized gastric epithelial cell line, the miR-19a levels were significantly increased (>1-fold) in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines, when the miR-19a expression level was normalized to U6 (Fig. 1; P<.05). Based on these results, the levels of miR-19a were significantly increased in human gastric carcinoma cells.


MicroRNA-19a mediates gastric carcinoma cell proliferation through the activation of nuclear factor-κB.

Yang F, Wang H, Jiang Z, Hu A, Chu L, Sun Y, Han J - Mol Med Rep (2015)

Expression levels of miR-19a in human gastric carcinoma cells. Reverse transcription-quantitative polymerase chain reaction analysis of the expression of miR-19a in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines and in the immortalized GES-1 gastric epithelial cell line. RNU48 was used as an endogenous control. Data are presented as the mean ± standard error of three independent experiments.*P<0.05, vs. control. miR, microRNA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581753&req=5

f1-mmr-12-04-5780: Expression levels of miR-19a in human gastric carcinoma cells. Reverse transcription-quantitative polymerase chain reaction analysis of the expression of miR-19a in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines and in the immortalized GES-1 gastric epithelial cell line. RNU48 was used as an endogenous control. Data are presented as the mean ± standard error of three independent experiments.*P<0.05, vs. control. miR, microRNA.
Mentions: The relative levels of miR-19a in human gastric carcinoma cells were detected using RT-qPCR. Compared with the GES-1 immortalized gastric epithelial cell line, the miR-19a levels were significantly increased (>1-fold) in the MGC-803, BGC-823 and SGC-7901 human gastric carcinoma cell lines, when the miR-19a expression level was normalized to U6 (Fig. 1; P<.05). Based on these results, the levels of miR-19a were significantly increased in human gastric carcinoma cells.

Bottom Line: The present study predominantly focussed on the effects of microRNA (miR)‑19a on NF‑κB activation.The results of the western blot analysis demonstrated that the protein levels of p65 increased when the MGC‑803 cells were transfected with miR‑19a mimics.In addition, the downstream target genes of miR‑19a, including intercellular adhesion molecule, vascular cell adhesion molecule and monocyte chemoattractant protein‑1, were upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Tumor Research and Therapy Center, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.

ABSTRACT
In gastric carcinoma, the nuclear factor‑κB (NF‑κB) signaling pathway is highly active, and the constitutive activation of NF‑κB prompts malignant cell proliferation. MicroRNAs are considered to be important mediators in the regulation of the NF‑κB signaling pathway. The present study predominantly focussed on the effects of microRNA (miR)‑19a on NF‑κB activation. Reverse transcription‑quantitative polymerase chain reaction was used to quantify the relative levels of miR‑19a in gastric carcinoma cells. MTT assays were used to determine the effect of miR‑19a on cellular proliferation. To detect the activation of NF‑κB, western blotting was performed to measure the protein levels of NF‑κB and the products of its downstream target genes. To define the target genes, luciferase reporter assays were used. miR‑19a was found to be markedly upregulated in gastric carcinoma cells. The overexpression of miR‑19a resulted in proliferation and enhanced migratory capabilities of the MGC‑803 gastric carcinoma cell line. The results of the western blot analysis demonstrated that the protein levels of p65 increased when the MGC‑803 cells were transfected with miR‑19a mimics. In addition, the downstream target genes of miR‑19a, including intercellular adhesion molecule, vascular cell adhesion molecule and monocyte chemoattractant protein‑1, were upregulated. The results of the luciferase assay indicated that IκB‑α was the target gene of miR‑19a. Therefore, the results of the present study suggested that miR‑19a enhances malignant gastric cell proliferation by constitutively activating the NF‑κB signaling pathway.

Show MeSH
Related in: MedlinePlus