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MiR-152 suppresses the proliferation and invasion of NSCLC cells by inhibiting FGF2.

Cheng Z, Ma R, Tan W, Zhang L - Exp. Mol. Med. (2014)

Bottom Line: MicroRNAs (miRNAs) regulate the proliferation and metastasis of cancer cells.Overexpression of miR-152 suppressed cell proliferation and colony formation and also limited migration and invasion.FGF2 knockdown suppressed cell proliferation, colony formation, migration and invasion, whereas FGF2 overexpression partially reversed the suppressive effect of miR-152.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiratory Medicine, ZhongNan Hospital of WuHan University, WuHan, China.

ABSTRACT
MicroRNAs (miRNAs) regulate the proliferation and metastasis of cancer cells. Here, we showed that miR-152 was downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. Overexpression of miR-152 suppressed cell proliferation and colony formation and also limited migration and invasion. Fibroblast growth factor 2 (FGF2) was confirmed as a direct target of miR-152. FGF2 knockdown suppressed cell proliferation, colony formation, migration and invasion, whereas FGF2 overexpression partially reversed the suppressive effect of miR-152. Furthermore, the presence of miR-152 was inversely correlated with FGF2 in NSCLC tissues. Overall, this study demonstrated that miR-152 suppressed the proliferation and invasion of NSCLC cells by downregulating FGF2. These findings provide novel insights with potential therapeutic applications for the treatment of NSCLC.

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Related in: MedlinePlus

MicroRNA-152 (miR-152) suppressed the proliferation of non-small-cell lung cancer (NSCLC) cells. (a) A549 cells were transfected with miR-152 or control mimics, and a cell viability assay (CCK-8) was performed. (b) Cell apoptosis assays. (c) Colony formation. (d) Expression of miR-152 in A549 cells transfected with miR-152 or control mimics. *P<0.05, **P<0.01 vs control.
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fig2: MicroRNA-152 (miR-152) suppressed the proliferation of non-small-cell lung cancer (NSCLC) cells. (a) A549 cells were transfected with miR-152 or control mimics, and a cell viability assay (CCK-8) was performed. (b) Cell apoptosis assays. (c) Colony formation. (d) Expression of miR-152 in A549 cells transfected with miR-152 or control mimics. *P<0.05, **P<0.01 vs control.

Mentions: To understand the role of miR-152 in the development of NSCLC, miR-152 was transfected into A549 cells, and we then used a CCK-8 assay to determine their proliferation. We found that miR-152 overexpression significantly suppressed A549 cell proliferation compared with their corresponding controls (Figure 2a). Next, flow cytometry was used to examine the apoptosis of A549 cells, and we found that miR-152 overexpression also induced this process (Figure 2b). We also used a colony formation assay to test the possibility that alterations in gene expression could cause either cell cycle arrest or cell death and lead to a reduction in colony number. Indeed, exogenous miR-152 expression significantly inhibited A549 colony formation (Figure 2c). The expression of miR-152 after transfection with a miR-152 mimic was determined by qRT-PCR (Figure 2d). Taken together, these results suggest that miR-152 was able to suppress NSCLC cell growth and induce apoptosis.


MiR-152 suppresses the proliferation and invasion of NSCLC cells by inhibiting FGF2.

Cheng Z, Ma R, Tan W, Zhang L - Exp. Mol. Med. (2014)

MicroRNA-152 (miR-152) suppressed the proliferation of non-small-cell lung cancer (NSCLC) cells. (a) A549 cells were transfected with miR-152 or control mimics, and a cell viability assay (CCK-8) was performed. (b) Cell apoptosis assays. (c) Colony formation. (d) Expression of miR-152 in A549 cells transfected with miR-152 or control mimics. *P<0.05, **P<0.01 vs control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150934&req=5

fig2: MicroRNA-152 (miR-152) suppressed the proliferation of non-small-cell lung cancer (NSCLC) cells. (a) A549 cells were transfected with miR-152 or control mimics, and a cell viability assay (CCK-8) was performed. (b) Cell apoptosis assays. (c) Colony formation. (d) Expression of miR-152 in A549 cells transfected with miR-152 or control mimics. *P<0.05, **P<0.01 vs control.
Mentions: To understand the role of miR-152 in the development of NSCLC, miR-152 was transfected into A549 cells, and we then used a CCK-8 assay to determine their proliferation. We found that miR-152 overexpression significantly suppressed A549 cell proliferation compared with their corresponding controls (Figure 2a). Next, flow cytometry was used to examine the apoptosis of A549 cells, and we found that miR-152 overexpression also induced this process (Figure 2b). We also used a colony formation assay to test the possibility that alterations in gene expression could cause either cell cycle arrest or cell death and lead to a reduction in colony number. Indeed, exogenous miR-152 expression significantly inhibited A549 colony formation (Figure 2c). The expression of miR-152 after transfection with a miR-152 mimic was determined by qRT-PCR (Figure 2d). Taken together, these results suggest that miR-152 was able to suppress NSCLC cell growth and induce apoptosis.

Bottom Line: MicroRNAs (miRNAs) regulate the proliferation and metastasis of cancer cells.Overexpression of miR-152 suppressed cell proliferation and colony formation and also limited migration and invasion.FGF2 knockdown suppressed cell proliferation, colony formation, migration and invasion, whereas FGF2 overexpression partially reversed the suppressive effect of miR-152.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiratory Medicine, ZhongNan Hospital of WuHan University, WuHan, China.

ABSTRACT
MicroRNAs (miRNAs) regulate the proliferation and metastasis of cancer cells. Here, we showed that miR-152 was downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. Overexpression of miR-152 suppressed cell proliferation and colony formation and also limited migration and invasion. Fibroblast growth factor 2 (FGF2) was confirmed as a direct target of miR-152. FGF2 knockdown suppressed cell proliferation, colony formation, migration and invasion, whereas FGF2 overexpression partially reversed the suppressive effect of miR-152. Furthermore, the presence of miR-152 was inversely correlated with FGF2 in NSCLC tissues. Overall, this study demonstrated that miR-152 suppressed the proliferation and invasion of NSCLC cells by downregulating FGF2. These findings provide novel insights with potential therapeutic applications for the treatment of NSCLC.

Show MeSH
Related in: MedlinePlus