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Mir-184 post-transcriptionally regulates SOX7 expression and promotes cell proliferation in human hepatocellular carcinoma.

Wu GG, Li WH, He WG, Jiang N, Zhang GX, Chen W, Yang HF, Liu QL, Huang YN, Zhang L, Zhang T, Zeng XC - PLoS ONE (2014)

Bottom Line: Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis.Overexpression of miR-184 in HCC cells increased cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-184 reduced cell proliferation, tumorigenicity, and cell cycle progression.Ectopic expression of miR-184 led to downregulation of the SOX7 protein, resulting in upregulation of c-Myc, Cyclin D1, and phosphorylation of Rb.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Zengcheng People's Hospital (BoJi-Affiliated Hospital of Sun Yat-Sen University), Zengcheng, China.

ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most common human malignancies and the third leading cause of cancer mortality worldwide. The development and progression of HCC is a complicated process, involving the deregulation of multiple genes that are essential to cell biological processes. Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis. Our study showed that miR-184 is upregulated in HCC cell lines and tissues. Overexpression of miR-184 in HCC cells increased cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-184 reduced cell proliferation, tumorigenicity, and cell cycle progression. Additionally, we identified SOX7 as a direct target of miR-184. Ectopic expression of miR-184 led to downregulation of the SOX7 protein, resulting in upregulation of c-Myc, Cyclin D1, and phosphorylation of Rb. Our findings suggested that miR-184 represents a potential onco-miR and plays an important role in HCC progression by suppressing SOX7 expression.

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Ectopic miR-184 promotes the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells stably overexpressing miR-184. B. Effects of ectopic miR-184 on the proliferation of the indicated HCC cell lines, as analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by the indicated HCC cell lines, 10 days after inoculation. D. Effects of ectopic miR-184 on the tumorigenicity of the indicated HCC cell lines, as determined by anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Effects of ectopic miR-184 on the cell cycle progression of the indicated HCC cells, as measured by flow cytometry analysis. Each bar represents the mean ± SD of three independent experiments. *P<0.05.
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pone-0088796-g002: Ectopic miR-184 promotes the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells stably overexpressing miR-184. B. Effects of ectopic miR-184 on the proliferation of the indicated HCC cell lines, as analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by the indicated HCC cell lines, 10 days after inoculation. D. Effects of ectopic miR-184 on the tumorigenicity of the indicated HCC cell lines, as determined by anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Effects of ectopic miR-184 on the cell cycle progression of the indicated HCC cells, as measured by flow cytometry analysis. Each bar represents the mean ± SD of three independent experiments. *P<0.05.

Mentions: To determine the effect of miR-184 on HCC progression, Hep3B and Huh7 cells stably overexpressing miR-184 were established for further study (Figure 2A). An MTT assay showed that ectopic expression of miR-184 significantly increased the growth rate of Hep3B and Huh7 cells (Figure 2B). Colony formation assays showed a similar result: overexpression of miR-184 enhanced the proliferation of HCC cells (Figure 2C). Additionally, an anchorage-independent growth assay revealed that Hep3B and Huh7 cells stably expressing miR-184 showed more and larger-sized colonies than control cells (Figure 2D). We further analyzed the cell cycle of Hep3B and Huh7 cells by flow cytometry. The results showed a dramatic decrease in the percentage of cells in G1/G0 phase and an increase in the percentage of cells in S phase (Figure 2E). The results suggested that upregulation of miR-184 promoted the proliferation and tumorigenicity of HCC cells in vitro.


Mir-184 post-transcriptionally regulates SOX7 expression and promotes cell proliferation in human hepatocellular carcinoma.

Wu GG, Li WH, He WG, Jiang N, Zhang GX, Chen W, Yang HF, Liu QL, Huang YN, Zhang L, Zhang T, Zeng XC - PLoS ONE (2014)

Ectopic miR-184 promotes the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells stably overexpressing miR-184. B. Effects of ectopic miR-184 on the proliferation of the indicated HCC cell lines, as analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by the indicated HCC cell lines, 10 days after inoculation. D. Effects of ectopic miR-184 on the tumorigenicity of the indicated HCC cell lines, as determined by anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Effects of ectopic miR-184 on the cell cycle progression of the indicated HCC cells, as measured by flow cytometry analysis. Each bar represents the mean ± SD of three independent experiments. *P<0.05.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3928300&req=5

pone-0088796-g002: Ectopic miR-184 promotes the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells stably overexpressing miR-184. B. Effects of ectopic miR-184 on the proliferation of the indicated HCC cell lines, as analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by the indicated HCC cell lines, 10 days after inoculation. D. Effects of ectopic miR-184 on the tumorigenicity of the indicated HCC cell lines, as determined by anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Effects of ectopic miR-184 on the cell cycle progression of the indicated HCC cells, as measured by flow cytometry analysis. Each bar represents the mean ± SD of three independent experiments. *P<0.05.
Mentions: To determine the effect of miR-184 on HCC progression, Hep3B and Huh7 cells stably overexpressing miR-184 were established for further study (Figure 2A). An MTT assay showed that ectopic expression of miR-184 significantly increased the growth rate of Hep3B and Huh7 cells (Figure 2B). Colony formation assays showed a similar result: overexpression of miR-184 enhanced the proliferation of HCC cells (Figure 2C). Additionally, an anchorage-independent growth assay revealed that Hep3B and Huh7 cells stably expressing miR-184 showed more and larger-sized colonies than control cells (Figure 2D). We further analyzed the cell cycle of Hep3B and Huh7 cells by flow cytometry. The results showed a dramatic decrease in the percentage of cells in G1/G0 phase and an increase in the percentage of cells in S phase (Figure 2E). The results suggested that upregulation of miR-184 promoted the proliferation and tumorigenicity of HCC cells in vitro.

Bottom Line: Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis.Overexpression of miR-184 in HCC cells increased cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-184 reduced cell proliferation, tumorigenicity, and cell cycle progression.Ectopic expression of miR-184 led to downregulation of the SOX7 protein, resulting in upregulation of c-Myc, Cyclin D1, and phosphorylation of Rb.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Zengcheng People's Hospital (BoJi-Affiliated Hospital of Sun Yat-Sen University), Zengcheng, China.

ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most common human malignancies and the third leading cause of cancer mortality worldwide. The development and progression of HCC is a complicated process, involving the deregulation of multiple genes that are essential to cell biological processes. Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis. Our study showed that miR-184 is upregulated in HCC cell lines and tissues. Overexpression of miR-184 in HCC cells increased cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-184 reduced cell proliferation, tumorigenicity, and cell cycle progression. Additionally, we identified SOX7 as a direct target of miR-184. Ectopic expression of miR-184 led to downregulation of the SOX7 protein, resulting in upregulation of c-Myc, Cyclin D1, and phosphorylation of Rb. Our findings suggested that miR-184 represents a potential onco-miR and plays an important role in HCC progression by suppressing SOX7 expression.

Show MeSH
Related in: MedlinePlus