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Downregulation of miR-106b induced breast cancer cell invasion and motility in association with overexpression of matrix metalloproteinase 2.

Ni X, Xia T, Zhao Y, Zhou W, Wu N, Liu X, Ding Q, Zha X, Sha J, Wang S - Cancer Sci. (2013)

Bottom Line: MMP2 was shown to be a direct target of miR-106b.Both gain- and loss-of-function studies showed that MMP2 could promote the migration and invasion of BC cells and that miR-106b could suppress both.The blockage of MMP2 by RNA interference mimicked the anti-migration and anti-invasion effects of miR-106b, and introduction of MMP2 antagonized the function of miR-106b.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China; State Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, China.

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Effects of miR-106b on the proliferation and apoptosis of breast cancer cells. (a) The growth of cells over 3 days was measured using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. The proliferation rate of miR-106b treated SUM1315-bo cells was significantly decreased compared with negative control treated SUM1315 cells. *P < 0.05. (b) Apoptosis was measured using flow cytometry. The miR-106b treated SUM1315-bo cells had a higher apoptosis rate than the negative control treated SUM1315-bo cells. *P < 0.05. (c) The proliferation rate of miR-106bI treated MCF-7 cells was significantly increased compared with negative control treated MCF-7 cells. *P < 0.05. (d) The miR-106bI treated MCF-7 cells had a lower apoptosis rate than the negative control treated MCF-7 cells. *P < 0.05.
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fig04: Effects of miR-106b on the proliferation and apoptosis of breast cancer cells. (a) The growth of cells over 3 days was measured using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. The proliferation rate of miR-106b treated SUM1315-bo cells was significantly decreased compared with negative control treated SUM1315 cells. *P < 0.05. (b) Apoptosis was measured using flow cytometry. The miR-106b treated SUM1315-bo cells had a higher apoptosis rate than the negative control treated SUM1315-bo cells. *P < 0.05. (c) The proliferation rate of miR-106bI treated MCF-7 cells was significantly increased compared with negative control treated MCF-7 cells. *P < 0.05. (d) The miR-106bI treated MCF-7 cells had a lower apoptosis rate than the negative control treated MCF-7 cells. *P < 0.05.

Mentions: To determine whether endogenous miR-106b can regulate tumor cell proliferation and apoptosis, we transfected SUM1315-bo cells with 200 nM miR-106b mimic or MCF-7 cells with 200 nM miR-106b inhibitor. Results showed a 0.76-fold decrease (Fig.4a) in proliferation and a 3.8-fold increase (Fig.4b) in cell apoptosis, respectively, after transfection of the miR-106b mimic. The proliferation of MCF7 cells increased 1.23-fold (Fig.4c) and the apoptosis of MCF7 cells decreased 1.56-fold (Fig.4d), respectively, after transfection with miR-106bI.


Downregulation of miR-106b induced breast cancer cell invasion and motility in association with overexpression of matrix metalloproteinase 2.

Ni X, Xia T, Zhao Y, Zhou W, Wu N, Liu X, Ding Q, Zha X, Sha J, Wang S - Cancer Sci. (2013)

Effects of miR-106b on the proliferation and apoptosis of breast cancer cells. (a) The growth of cells over 3 days was measured using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. The proliferation rate of miR-106b treated SUM1315-bo cells was significantly decreased compared with negative control treated SUM1315 cells. *P < 0.05. (b) Apoptosis was measured using flow cytometry. The miR-106b treated SUM1315-bo cells had a higher apoptosis rate than the negative control treated SUM1315-bo cells. *P < 0.05. (c) The proliferation rate of miR-106bI treated MCF-7 cells was significantly increased compared with negative control treated MCF-7 cells. *P < 0.05. (d) The miR-106bI treated MCF-7 cells had a lower apoptosis rate than the negative control treated MCF-7 cells. *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig04: Effects of miR-106b on the proliferation and apoptosis of breast cancer cells. (a) The growth of cells over 3 days was measured using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. The proliferation rate of miR-106b treated SUM1315-bo cells was significantly decreased compared with negative control treated SUM1315 cells. *P < 0.05. (b) Apoptosis was measured using flow cytometry. The miR-106b treated SUM1315-bo cells had a higher apoptosis rate than the negative control treated SUM1315-bo cells. *P < 0.05. (c) The proliferation rate of miR-106bI treated MCF-7 cells was significantly increased compared with negative control treated MCF-7 cells. *P < 0.05. (d) The miR-106bI treated MCF-7 cells had a lower apoptosis rate than the negative control treated MCF-7 cells. *P < 0.05.
Mentions: To determine whether endogenous miR-106b can regulate tumor cell proliferation and apoptosis, we transfected SUM1315-bo cells with 200 nM miR-106b mimic or MCF-7 cells with 200 nM miR-106b inhibitor. Results showed a 0.76-fold decrease (Fig.4a) in proliferation and a 3.8-fold increase (Fig.4b) in cell apoptosis, respectively, after transfection of the miR-106b mimic. The proliferation of MCF7 cells increased 1.23-fold (Fig.4c) and the apoptosis of MCF7 cells decreased 1.56-fold (Fig.4d), respectively, after transfection with miR-106bI.

Bottom Line: MMP2 was shown to be a direct target of miR-106b.Both gain- and loss-of-function studies showed that MMP2 could promote the migration and invasion of BC cells and that miR-106b could suppress both.The blockage of MMP2 by RNA interference mimicked the anti-migration and anti-invasion effects of miR-106b, and introduction of MMP2 antagonized the function of miR-106b.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China; State Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, China.

Show MeSH
Related in: MedlinePlus