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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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Inhibition of miR-184 reduces the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells transfected with miR-184 inhibitor. B. The proliferation ability of HCC cells transfected with an miR-184 inhibitor or negative control (NC), analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by indicated HCC cell lines, 10 days after inoculation. D. The tumorigenicity of HCC cells transfected with miR-184 inhibitor or NC, as determined by an anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Flow cytometry analysis of indicated HCC cells transfected with miR-184-inhibitor or NC. Each bar represents the mean ± SD of three independent experiments. *P<0.05.
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pone-0088796-g003: Inhibition of miR-184 reduces the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells transfected with miR-184 inhibitor. B. The proliferation ability of HCC cells transfected with an miR-184 inhibitor or negative control (NC), analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by indicated HCC cell lines, 10 days after inoculation. D. The tumorigenicity of HCC cells transfected with miR-184 inhibitor or NC, as determined by an anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Flow cytometry analysis of indicated HCC cells transfected with miR-184-inhibitor or NC. Each bar represents the mean ± SD of three independent experiments. *P<0.05.

Mentions: To further test whether endogenous miR-184 helps to sustain the proliferative property of HCC cells, loss-of-function studies using a miR-184 inhibitor were performed (Figure 3A). The results showed that suppression of miR-184 significantly decreased the growth rate of Hep3B, Huh7 and THLE3, when transfected with the miR-184 inhibitor, compared with that of NC transfected cells (Figure 3, B and C, and Figure S2A). The anchorage-independent growth assay revealed that Hep3B-miR-184-inhibitor and Huh7-miR-184-inhibitor cells produced fewer and smaller colonies than the negative control cells, indicating the inhibitory function of the miR-184 inhibitor on HCC tumorigenicity (Figure 3D). In addition, flow cytometry showed a significant increase in the percentage of cells in G1/G0 phase and a decrease in the percentage of cells in S phase in cells transfected with the miR-184 inhibitor compared with NC transfected cells (Figure 3E). These results suggested that downregulation of miR-184 could reduce the proliferation and tumorigenicity of HCC cells.


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)

Inhibition of miR-184 reduces the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells transfected with miR-184 inhibitor. B. The proliferation ability of HCC cells transfected with an miR-184 inhibitor or negative control (NC), analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by indicated HCC cell lines, 10 days after inoculation. D. The tumorigenicity of HCC cells transfected with miR-184 inhibitor or NC, as determined by an anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Flow cytometry analysis of indicated HCC cells transfected with miR-184-inhibitor or NC. 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-g003: Inhibition of miR-184 reduces the proliferation of HCC cells.A. Real-time PCR analysis of miR-184 expression in Hep3B and Huh7 cells transfected with miR-184 inhibitor. B. The proliferation ability of HCC cells transfected with an miR-184 inhibitor or negative control (NC), analyzed by the MTT assay. C. Representative micrographs (left) and quantifications (right) of crystal violet stained cell colonies formed by indicated HCC cell lines, 10 days after inoculation. D. The tumorigenicity of HCC cells transfected with miR-184 inhibitor or NC, as determined by an anchorage-independent growth ability assay. Colonies larger than 0.1 mm were scored. E. Flow cytometry analysis of indicated HCC cells transfected with miR-184-inhibitor or NC. Each bar represents the mean ± SD of three independent experiments. *P<0.05.
Mentions: To further test whether endogenous miR-184 helps to sustain the proliferative property of HCC cells, loss-of-function studies using a miR-184 inhibitor were performed (Figure 3A). The results showed that suppression of miR-184 significantly decreased the growth rate of Hep3B, Huh7 and THLE3, when transfected with the miR-184 inhibitor, compared with that of NC transfected cells (Figure 3, B and C, and Figure S2A). The anchorage-independent growth assay revealed that Hep3B-miR-184-inhibitor and Huh7-miR-184-inhibitor cells produced fewer and smaller colonies than the negative control cells, indicating the inhibitory function of the miR-184 inhibitor on HCC tumorigenicity (Figure 3D). In addition, flow cytometry showed a significant increase in the percentage of cells in G1/G0 phase and a decrease in the percentage of cells in S phase in cells transfected with the miR-184 inhibitor compared with NC transfected cells (Figure 3E). These results suggested that downregulation of miR-184 could reduce the proliferation and tumorigenicity of HCC cells.

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