Downregulation of miR-93 inhibits cell proliferation an

MicroRNA-93 promotes the malignant phenotypes of human glioma cells and induces their chemoresistance to temozolomide. Chen R, Liu H, Cheng Q, Jiang B, Peng R, Zou Q, Yang W, Yang X, Wu X, Chen Z - Biol Open (2016) Bottom Line: Moreover, the upregulated miR-93 level was significantly associated with the advanced malignancy.We also found that upregulation of miR-93 promoted the proliferation, migration and invasion of glioma cells, and that miR-93 was involved in the regulation of cell cycle progression by mediating the protein levels of P21, P27, P53 and Cyclin D1.Knockdown of P21 attenuated the suppressive effects of miR-93 inhibition on cell cycle progression and colony formation. View Article: PubMed Central - PubMed Affiliation: Department of Neurosurgery, Nanhua Hospital Affiliated to Nanhua University, Hengyang, Hunan 421001, China. No MeSH data available. Related in: MedlinePlus	© Copyright Policy - open-access Related In: Results - Collection License Show All Figures getmorefigures.php?uid=PMC4920179&req=5 BIO015552F2: Downregulation of miR-93 inhibits cell proliferation and arrests cell cycle in U87 and SF126 cells. (A,B) Real-time RT-PCR was performed to analyze the miR-93 levels in several glioma cell lines including U87, U251, SF126, SF767, A172 and SHG44 (A), and in U87 and SF126 cells transfected with miR-93 inhibitor or mimic, respectively (B). Cells transfected with scramble miRNA (miR-NC) were used as control. (C,D) MTT assay was performed to determine the cell proliferation in U87 cells (C) and SF126 cells (D) after miR-93 inhibitor or mimic transfection. (E,F) Cell cycle analysis was performed to examine the cell cycle distribution in U87 cells (E) and SF126 cells (F) after miR-93 inhibitor or mimic transfection. Data represented as mean±s.d; P<0.05, P<0.01, P<0.001 vs miR-NC. Mentions:** In vitro study was further performed to investigate the detailed role of miR-93 in glioma. Its expression levels were firstly examined in several common glioma cell lines including U87, U251, SF126, SF767, A172 and SHG44 by conducting real-time RT-PCR. As indicated in Fig. 2A, U87 cells showed the highest miR-93 levels, while SF126 cells showed the lowest miR-93 levels. Therefore, we used U87 and SF126 cell lines in the following experiments. To knockdown the miR-93 levels in U87 cells, they were transfected with inhibitor. As demonstrated in Fig. 2B, transfection with miR-93 inhibitor led to a significant decrease in the mir-93 levels in U87 cells, when compared to the non-transfected U87 cells. To upregulate the miR-93 levels in SF126 cells, miR-93 mimic was used. Transfection with miR-93 mimic significantly enhanced the miR-93 levels in SF126 cells compared to control group. MTT assay was further conducted to examine cell proliferation. We observed that inhibition of miR-93 expression caused a significantly reduction in U87 cell proliferation, while overexpression of miR-93 markedly promoted SF126 cell proliferation (Fig. 2C,D). We further examined the cell cycle distribution. Knockdown of miR-93 in U87 cells significantly induced a cell cycle arrest at G0/G1 stage (Fig. 2E), while overexpression of miR-93 promoted the cell cycle progression in SF126 cells (Fig. 2F). These findings suggest that miR-93 plays an oncogenic role in the growth of glioma probably via promoting the cell cycle progression.Fig. 2.

MicroRNA-93 promotes the malignant phenotypes of human glioma cells and induces their chemoresistance to temozolomide.

Chen R, Liu H, Cheng Q, Jiang B, Peng R, Zou Q, Yang W, Yang X, Wu X, Chen Z - Biol Open (2016)

Bottom Line: Moreover, the upregulated miR-93 level was significantly associated with the advanced malignancy.We also found that upregulation of miR-93 promoted the proliferation, migration and invasion of glioma cells, and that miR-93 was involved in the regulation of cell cycle progression by mediating the protein levels of P21, P27, P53 and Cyclin D1.Knockdown of P21 attenuated the suppressive effects of miR-93 inhibition on cell cycle progression and colony formation.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Nanhua Hospital Affiliated to Nanhua University, Hengyang, Hunan 421001, China.

No MeSH data available.

Related in: MedlinePlus

Downregulation of miR-93 inhibits cell proliferation and arrests cell cycle in U87 and SF126 cells. (A,B) Real-time RT-PCR was performed to analyze the miR-93 levels in several glioma cell lines including U87, U251, SF126, SF767, A172 and SHG44 (A), and in U87 and SF126 cells transfected with miR-93 inhibitor or mimic, respectively (B). Cells transfected with scramble miRNA (miR-NC) were used as control. (C,D) MTT assay was performed to determine the cell proliferation in U87 cells (C) and SF126 cells (D) after miR-93 inhibitor or mimic transfection. (E,F) Cell cycle analysis was performed to examine the cell cycle distribution in U87 cells (E) and SF126 cells (F) after miR-93 inhibitor or mimic transfection. Data represented as mean±s.d; *P<0.05, **P<0.01, ***P<0.001 vs miR-NC.

Related In: Results - Collection

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BIO015552F2: Downregulation of miR-93 inhibits cell proliferation and arrests cell cycle in U87 and SF126 cells. (A,B) Real-time RT-PCR was performed to analyze the miR-93 levels in several glioma cell lines including U87, U251, SF126, SF767, A172 and SHG44 (A), and in U87 and SF126 cells transfected with miR-93 inhibitor or mimic, respectively (B). Cells transfected with scramble miRNA (miR-NC) were used as control. (C,D) MTT assay was performed to determine the cell proliferation in U87 cells (C) and SF126 cells (D) after miR-93 inhibitor or mimic transfection. (E,F) Cell cycle analysis was performed to examine the cell cycle distribution in U87 cells (E) and SF126 cells (F) after miR-93 inhibitor or mimic transfection. Data represented as mean±s.d; *P<0.05, **P<0.01, ***P<0.001 vs miR-NC.

Mentions: In vitro study was further performed to investigate the detailed role of miR-93 in glioma. Its expression levels were firstly examined in several common glioma cell lines including U87, U251, SF126, SF767, A172 and SHG44 by conducting real-time RT-PCR. As indicated in Fig. 2A, U87 cells showed the highest miR-93 levels, while SF126 cells showed the lowest miR-93 levels. Therefore, we used U87 and SF126 cell lines in the following experiments. To knockdown the miR-93 levels in U87 cells, they were transfected with inhibitor. As demonstrated in Fig. 2B, transfection with miR-93 inhibitor led to a significant decrease in the mir-93 levels in U87 cells, when compared to the non-transfected U87 cells. To upregulate the miR-93 levels in SF126 cells, miR-93 mimic was used. Transfection with miR-93 mimic significantly enhanced the miR-93 levels in SF126 cells compared to control group. MTT assay was further conducted to examine cell proliferation. We observed that inhibition of miR-93 expression caused a significantly reduction in U87 cell proliferation, while overexpression of miR-93 markedly promoted SF126 cell proliferation (Fig. 2C,D). We further examined the cell cycle distribution. Knockdown of miR-93 in U87 cells significantly induced a cell cycle arrest at G0/G1 stage (Fig. 2E), while overexpression of miR-93 promoted the cell cycle progression in SF126 cells (Fig. 2F). These findings suggest that miR-93 plays an oncogenic role in the growth of glioma probably via promoting the cell cycle progression.Fig. 2.