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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

Fibroblast growth factor 2 (FGF2) inhibition resulted in similar effects as microRNA-152 (miR-152) overexpression. (a) The viability of A549 cells transfected with FGF2 or control short hairpin RNAs (shRNAs) was detected using CCK-8. (b) In vitro migration. (c) In vitro invasion. (d) Expression of FGF2 mRNA was detected by quantitative real-time PCR (qRT-PCR) in A549 cells transfected with shRNA-NC or shRNA-FGF2. (e) FGF2 protein levels were detected by western blot analysis in A549 cells transfected with FGF2 or control shRNA. *P<0.05, **P<0.01 vs control.
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fig5: Fibroblast growth factor 2 (FGF2) inhibition resulted in similar effects as microRNA-152 (miR-152) overexpression. (a) The viability of A549 cells transfected with FGF2 or control short hairpin RNAs (shRNAs) was detected using CCK-8. (b) In vitro migration. (c) In vitro invasion. (d) Expression of FGF2 mRNA was detected by quantitative real-time PCR (qRT-PCR) in A549 cells transfected with shRNA-NC or shRNA-FGF2. (e) FGF2 protein levels were detected by western blot analysis in A549 cells transfected with FGF2 or control shRNA. *P<0.05, **P<0.01 vs control.

Mentions: Because we found that FGF2 is a direct target of miR-152, we further investigated whether FGF2 silencing by shRNA could induce effects on NSCLC cells similar to those caused by the overexpression of miR-152. A549 cells were transfected with either an shRNA targeted against FGF2 or a nontargeting control. The inhibition of FGF2 by shRNA significantly suppressed the proliferation, migration and invasion of A549 cells (Figures 5a–c). Western blotting and qRT-PCR were used to detect the effects of FGF2 shRNA (Figures 5d and e). These data indicate that inhibition of FGF2 mimicked the effects of miR-152 overexpression.


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)

Fibroblast growth factor 2 (FGF2) inhibition resulted in similar effects as microRNA-152 (miR-152) overexpression. (a) The viability of A549 cells transfected with FGF2 or control short hairpin RNAs (shRNAs) was detected using CCK-8. (b) In vitro migration. (c) In vitro invasion. (d) Expression of FGF2 mRNA was detected by quantitative real-time PCR (qRT-PCR) in A549 cells transfected with shRNA-NC or shRNA-FGF2. (e) FGF2 protein levels were detected by western blot analysis in A549 cells transfected with FGF2 or control shRNA. *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

fig5: Fibroblast growth factor 2 (FGF2) inhibition resulted in similar effects as microRNA-152 (miR-152) overexpression. (a) The viability of A549 cells transfected with FGF2 or control short hairpin RNAs (shRNAs) was detected using CCK-8. (b) In vitro migration. (c) In vitro invasion. (d) Expression of FGF2 mRNA was detected by quantitative real-time PCR (qRT-PCR) in A549 cells transfected with shRNA-NC or shRNA-FGF2. (e) FGF2 protein levels were detected by western blot analysis in A549 cells transfected with FGF2 or control shRNA. *P<0.05, **P<0.01 vs control.
Mentions: Because we found that FGF2 is a direct target of miR-152, we further investigated whether FGF2 silencing by shRNA could induce effects on NSCLC cells similar to those caused by the overexpression of miR-152. A549 cells were transfected with either an shRNA targeted against FGF2 or a nontargeting control. The inhibition of FGF2 by shRNA significantly suppressed the proliferation, migration and invasion of A549 cells (Figures 5a–c). Western blotting and qRT-PCR were used to detect the effects of FGF2 shRNA (Figures 5d and e). These data indicate that inhibition of FGF2 mimicked the effects of miR-152 overexpression.

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