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MicroRNA-495 induces breast cancer cell migration by targeting JAM-A.

Cao M, Nie W, Li J, Zhang Y, Yan X, Guan X, Chen X, Zen K, Zhang CY, Jiang X, Hou D - Protein Cell (2014)

Bottom Line: MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression.In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR).Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for microRNA Biology and Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210093, China.

ABSTRACT
MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.

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Effects of miR-495 on breast cancer cell migration. (A) Left panel: Representative image of wound healing assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (B) Left panel: Representative image of Transwell assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. (C) Left panel: Representative image of wound healing assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (D) Left panel: Representative image of Transwell assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. *P < 0.05; **P < 0.01
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Fig4: Effects of miR-495 on breast cancer cell migration. (A) Left panel: Representative image of wound healing assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (B) Left panel: Representative image of Transwell assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. (C) Left panel: Representative image of wound healing assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (D) Left panel: Representative image of Transwell assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. *P < 0.05; **P < 0.01

Mentions: After establishing that JAM-A is involved in the migration of breast cancer cells, the biological significance of miR-495 in breast cancer was then investigated. As shown by wound healing assays in Fig. 4A, more MCF-7 cells migrated into the scratch on the cell monolayer when transfected with miR-495 mimic; consistently, knockdown of miR-495 by miRNA inhibitor showed the opposite effects. The same biological function of miR-495 was found in MDA-MB-231 cells (Fig. 4C). In addition, Transwell assays revealed a significant increase in cells migrating through the membrane when MCF-7 cells and MDA-MB-231 cells were transfected with miR-495 mimic (Fig. 4B and 4D). As anticipated, the mobility of MCF-7 and MDA-MB-231 cells was clearly inhibited by transfection with miR-495 inhibitor, shown by Fig. 4B and 4D, respectively.Figure 4


MicroRNA-495 induces breast cancer cell migration by targeting JAM-A.

Cao M, Nie W, Li J, Zhang Y, Yan X, Guan X, Chen X, Zen K, Zhang CY, Jiang X, Hou D - Protein Cell (2014)

Effects of miR-495 on breast cancer cell migration. (A) Left panel: Representative image of wound healing assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (B) Left panel: Representative image of Transwell assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. (C) Left panel: Representative image of wound healing assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (D) Left panel: Representative image of Transwell assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. *P < 0.05; **P < 0.01
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Fig4: Effects of miR-495 on breast cancer cell migration. (A) Left panel: Representative image of wound healing assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (B) Left panel: Representative image of Transwell assay of MCF-7 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. (C) Left panel: Representative image of wound healing assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the wound closure rates. (D) Left panel: Representative image of Transwell assay of MDA-MB-231 cells transfected with control mimic, miR-495 mimic, control inhibitor or miR-495 inhibitor. Right panel: Quantitative analysis of the migration rates. *P < 0.05; **P < 0.01
Mentions: After establishing that JAM-A is involved in the migration of breast cancer cells, the biological significance of miR-495 in breast cancer was then investigated. As shown by wound healing assays in Fig. 4A, more MCF-7 cells migrated into the scratch on the cell monolayer when transfected with miR-495 mimic; consistently, knockdown of miR-495 by miRNA inhibitor showed the opposite effects. The same biological function of miR-495 was found in MDA-MB-231 cells (Fig. 4C). In addition, Transwell assays revealed a significant increase in cells migrating through the membrane when MCF-7 cells and MDA-MB-231 cells were transfected with miR-495 mimic (Fig. 4B and 4D). As anticipated, the mobility of MCF-7 and MDA-MB-231 cells was clearly inhibited by transfection with miR-495 inhibitor, shown by Fig. 4B and 4D, respectively.Figure 4

Bottom Line: MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression.In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR).Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for microRNA Biology and Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210093, China.

ABSTRACT
MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.

Show MeSH
Related in: MedlinePlus