Limits...
MicroRNA-153 inhibits osteosarcoma cells proliferation and invasion by targeting TGF-β2.

Niu G, Li B, Sun L, An C - PLoS ONE (2015)

Bottom Line: Our results further revealed that transforming growth factor beta 2 (TGF-β2) was negatively regulated by miR-153.Furthermore, overexpression of miR-153 decreased p-SMAD2, p-SMAD3, epidermal growth factor receptor (EGFR) and insulin-like growth factor binding protein-3 (IGFBP-3) expressions, which were the downstream signaling molecules of TGF-β.Furthermore, miRNA-153 suppressed TGF-β-mediated MG-63 proliferation and migration.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, Shandong Provincial Hospital affiliated to Shandong University, Shandong University, Jinan, P.R. China.

ABSTRACT
Increasing evidence indicates that microRNAs (miRNAs), a class of small noncoding RNAs, participate in almost every step of cellular processes. MiRNAs are aberrantly expressed in human cancers and contribute to cancer development and progression. Study of miRNAs may provide a new clue for understanding the mechanism of carcinogenesis and a new tool for cancer treatment. In the present study, miR-153 was downregulated in human osteosarcoma tissues and cell lines. Introduction of miR-153 mimics into the MG-63 cells inhibited cell proliferation and invasion. Our results further revealed that transforming growth factor beta 2 (TGF-β2) was negatively regulated by miR-153. Furthermore, overexpression of miR-153 decreased p-SMAD2, p-SMAD3, epidermal growth factor receptor (EGFR) and insulin-like growth factor binding protein-3 (IGFBP-3) expressions, which were the downstream signaling molecules of TGF-β. Furthermore, miRNA-153 suppressed TGF-β-mediated MG-63 proliferation and migration. Therefore, our results suggest that miR-153 may act as a tumor suppressor in osteosarcoma through targeting TGF-β2.

No MeSH data available.


Related in: MedlinePlus

TGF-β2 was a direct target of miR-153 in osteosarcoma cells.(A) Computer prediction of miR-153 binding sites in the 3’UTR of human TGF-β2 gene. (B) Expression of TGF-β2 mRNA was examined by qRT-PCR in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. The expression of TGF-β2 was normalized to GAPDH. (C) MG-63cells were co-transfected with miR-153 and WT or MUT 3’UTR of TGF-β2. (D) Protein level was detected by Western blotting in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. GAPDH was also detected as a loading control. ***p<0.001.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4368543&req=5

pone.0119225.g003: TGF-β2 was a direct target of miR-153 in osteosarcoma cells.(A) Computer prediction of miR-153 binding sites in the 3’UTR of human TGF-β2 gene. (B) Expression of TGF-β2 mRNA was examined by qRT-PCR in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. The expression of TGF-β2 was normalized to GAPDH. (C) MG-63cells were co-transfected with miR-153 and WT or MUT 3’UTR of TGF-β2. (D) Protein level was detected by Western blotting in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. GAPDH was also detected as a loading control. ***p<0.001.

Mentions: TGF-β2 was predicted to be a target of miR-153 (Fig. 3A). The mRNA level of TGF-β2 was inhibited in the miR-153 mimic group (Fig. 3B). MiR-153 significantly suppressed the luciferase activity of WT 3’UTR, but not the MUT 3’UTR of TGF-β2 in MG-63 cells (Fig. 3C). Overexpression of miR-153 can also suppress TGF-β2 protein levels (Fig. 3D).


MicroRNA-153 inhibits osteosarcoma cells proliferation and invasion by targeting TGF-β2.

Niu G, Li B, Sun L, An C - PLoS ONE (2015)

TGF-β2 was a direct target of miR-153 in osteosarcoma cells.(A) Computer prediction of miR-153 binding sites in the 3’UTR of human TGF-β2 gene. (B) Expression of TGF-β2 mRNA was examined by qRT-PCR in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. The expression of TGF-β2 was normalized to GAPDH. (C) MG-63cells were co-transfected with miR-153 and WT or MUT 3’UTR of TGF-β2. (D) Protein level was detected by Western blotting in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. GAPDH was also detected as a loading control. ***p<0.001.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4368543&req=5

pone.0119225.g003: TGF-β2 was a direct target of miR-153 in osteosarcoma cells.(A) Computer prediction of miR-153 binding sites in the 3’UTR of human TGF-β2 gene. (B) Expression of TGF-β2 mRNA was examined by qRT-PCR in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. The expression of TGF-β2 was normalized to GAPDH. (C) MG-63cells were co-transfected with miR-153 and WT or MUT 3’UTR of TGF-β2. (D) Protein level was detected by Western blotting in MG-63 cells transfected with miR-153 mimic or the scramble mimics or no treat. GAPDH was also detected as a loading control. ***p<0.001.
Mentions: TGF-β2 was predicted to be a target of miR-153 (Fig. 3A). The mRNA level of TGF-β2 was inhibited in the miR-153 mimic group (Fig. 3B). MiR-153 significantly suppressed the luciferase activity of WT 3’UTR, but not the MUT 3’UTR of TGF-β2 in MG-63 cells (Fig. 3C). Overexpression of miR-153 can also suppress TGF-β2 protein levels (Fig. 3D).

Bottom Line: Our results further revealed that transforming growth factor beta 2 (TGF-β2) was negatively regulated by miR-153.Furthermore, overexpression of miR-153 decreased p-SMAD2, p-SMAD3, epidermal growth factor receptor (EGFR) and insulin-like growth factor binding protein-3 (IGFBP-3) expressions, which were the downstream signaling molecules of TGF-β.Furthermore, miRNA-153 suppressed TGF-β-mediated MG-63 proliferation and migration.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, Shandong Provincial Hospital affiliated to Shandong University, Shandong University, Jinan, P.R. China.

ABSTRACT
Increasing evidence indicates that microRNAs (miRNAs), a class of small noncoding RNAs, participate in almost every step of cellular processes. MiRNAs are aberrantly expressed in human cancers and contribute to cancer development and progression. Study of miRNAs may provide a new clue for understanding the mechanism of carcinogenesis and a new tool for cancer treatment. In the present study, miR-153 was downregulated in human osteosarcoma tissues and cell lines. Introduction of miR-153 mimics into the MG-63 cells inhibited cell proliferation and invasion. Our results further revealed that transforming growth factor beta 2 (TGF-β2) was negatively regulated by miR-153. Furthermore, overexpression of miR-153 decreased p-SMAD2, p-SMAD3, epidermal growth factor receptor (EGFR) and insulin-like growth factor binding protein-3 (IGFBP-3) expressions, which were the downstream signaling molecules of TGF-β. Furthermore, miRNA-153 suppressed TGF-β-mediated MG-63 proliferation and migration. Therefore, our results suggest that miR-153 may act as a tumor suppressor in osteosarcoma through targeting TGF-β2.

No MeSH data available.


Related in: MedlinePlus