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Tumor-suppressive microRNA-218 inhibits cancer cell migration and invasion via targeting of LASP1 in prostate cancer.

Nishikawa R, Goto Y, Sakamoto S, Chiyomaru T, Enokida H, Kojima S, Kinoshita T, Yamamoto N, Nakagawa M, Naya Y, Ichikawa T, Seki N - Cancer Sci. (2014)

Bottom Line: Our recent studies of the microRNA (miRNA) expression signature in prostate cancer (PCa) indicated that miRNA-218 (miR-218) was significantly downregulated in clinical specimens, suggesting that miR-218 might act as a tumor-suppressive miRNA in PCa.LASP1 is a cytoskeletal scaffold protein that plays critical roles in cytoskeletal organization and cell migration.Our data on pathways regulated by tumor-suppressive miR-218 provide new insight into the potential mechanisms of PCa oncogenesis and metastasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Functional Genomics, Chiba, Japan; Department of Urology, Chiba University Graduate School of Medicine, Chiba, Japan.

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The expression levels of miR-218 in clinical specimens and prostate cancer (PCa) cell lines (PC3 and DU145). Real-time PCR showed that the expression levels of miR-218 were significantly lower in PCa tissues and cell lines than in normal prostate tissues. RNU48 was used as an internal control.
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fig01: The expression levels of miR-218 in clinical specimens and prostate cancer (PCa) cell lines (PC3 and DU145). Real-time PCR showed that the expression levels of miR-218 were significantly lower in PCa tissues and cell lines than in normal prostate tissues. RNU48 was used as an internal control.

Mentions: To validate our past miRNA profiling results, we evaluated the expression levels of miR-218 in 17 radical prostatectomy specimens. Quantitative stem-loop RT-PCR demonstrated that miR-218 expression was significantly lower in clinical PCa specimens and PCa cell lines (PC3 and DU145) compared with non-cancerous specimens (Fig. 1). The typical FFPE specimens used for expression analysis in this study are shown in Fig. S1.


Tumor-suppressive microRNA-218 inhibits cancer cell migration and invasion via targeting of LASP1 in prostate cancer.

Nishikawa R, Goto Y, Sakamoto S, Chiyomaru T, Enokida H, Kojima S, Kinoshita T, Yamamoto N, Nakagawa M, Naya Y, Ichikawa T, Seki N - Cancer Sci. (2014)

The expression levels of miR-218 in clinical specimens and prostate cancer (PCa) cell lines (PC3 and DU145). Real-time PCR showed that the expression levels of miR-218 were significantly lower in PCa tissues and cell lines than in normal prostate tissues. RNU48 was used as an internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317931&req=5

fig01: The expression levels of miR-218 in clinical specimens and prostate cancer (PCa) cell lines (PC3 and DU145). Real-time PCR showed that the expression levels of miR-218 were significantly lower in PCa tissues and cell lines than in normal prostate tissues. RNU48 was used as an internal control.
Mentions: To validate our past miRNA profiling results, we evaluated the expression levels of miR-218 in 17 radical prostatectomy specimens. Quantitative stem-loop RT-PCR demonstrated that miR-218 expression was significantly lower in clinical PCa specimens and PCa cell lines (PC3 and DU145) compared with non-cancerous specimens (Fig. 1). The typical FFPE specimens used for expression analysis in this study are shown in Fig. S1.

Bottom Line: Our recent studies of the microRNA (miRNA) expression signature in prostate cancer (PCa) indicated that miRNA-218 (miR-218) was significantly downregulated in clinical specimens, suggesting that miR-218 might act as a tumor-suppressive miRNA in PCa.LASP1 is a cytoskeletal scaffold protein that plays critical roles in cytoskeletal organization and cell migration.Our data on pathways regulated by tumor-suppressive miR-218 provide new insight into the potential mechanisms of PCa oncogenesis and metastasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Functional Genomics, Chiba, Japan; Department of Urology, Chiba University Graduate School of Medicine, Chiba, Japan.

Show MeSH
Related in: MedlinePlus