microRNA-133 inhibits cell proliferation, migration and invasion in prostate cancer cells by targeting the epidermal growth factor receptor.
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):1967-75. doi: 10.3892/or.. Epub
2012 Mar 7.microRNA-133 inhibits cell proliferation, migration and invasion in
prostate cancer cells by targeting the epidermal growth factor receptor.1, , , , , , , .1Department of Urology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, PR China.AbstractIt has been shown that regulation of EGFR expression in prostate cancer
cells is mostly at the transcriptional level. microRNA-133 (miR-133) has long
been recognized as a muscle-specific miRNA which may regulate myoblast differentiation
and participate in many myogenic diseases. Recently, it has been reported that
miR-133 is also involved in other tumors, such as bladder cancer, esophageal cancer
and may regulate cell motility in these cancer cells. In the present study, we
examined the expression and effects of miR-133 in two hormone-insensitive prostate
cancer cell lines. The expression of miR-133a and miR-133b were analyzed by quantitative
RT-PCR. After transfection of miR-133a and miR-133b, cell viability assay, luciferase
assay, western blot analysis, cell migration and invasion assay were conducted
in Du145 and PC3 cells. In this study, we showed that miR-133a and miR-133b are
expressed at the detection limit in two hormone-insensitive prostate cancer cell
lines, PC3 and DU145. Ectopic expression of miR-133 inhibited cell proliferation,
migration and invasion in these cells. We also provide the first evidence that
miR-133 may target EGFR. Our study provided the first glimpse of the functional
role of miR-133 in two hormone-independent prostate cancer cell lines. These results
may add to our knowledge on the molecular basis of prostate cancer progression.PMID:
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External link. Please review our .miR-125b inhibits osteoblastic differentiation by down-regulation of cell proliferation.
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2008 Apr 4;368(2):267-72. doi: 10.1016/j.bbrc.. Epub
2008 Jan 28.miR-125b inhibits osteoblastic differentiation by down-regulation of cell proliferation.1, , , , , , , , , , , , .1Division of Functional Genomics & Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka City, Saitama 350-1241, Japan.AbstractAlthough various microRNAs regulate cell differentiation and proliferation, no miRNA has been reported so far to play an important role in the regulation of osteoblast differentiation. Here we describe the role of miR-125b in osteoblastic differentiation in mouse mesenchymal stem cells, ST2, by regulating cell proliferation. The expression of miR-125b was time-dependently increased in ST2 cells, and the increase in miR-125b expression was attenuated in osteoblastic-differentiated ST2 cells induced by BMP-4. The transfection of exogenous miR-125b inhibited proliferation of ST2 cells and caused inhibition of osteoblastic differentiation. In contrast, when the endogenous miR-125b was blocked by transfection of its antisense RNA molecule, alkaline phosphatase activity after BMP-4 treatment was elevated. These results strongly suggest that miR-125b is involved in osteoblastic differentiation through the regulation of cell proliferation.PMID:
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External link. Please review our .MicroRNA-142-3p inhibits cell proliferation and invasion of cervical cancer cells by targeting FZD7.
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):8065-73. doi: 10.-015-3483-2. Epub
2015 May 15.MicroRNA-142-3p inhibits cell proliferation and invasion of cervical cancer cells by targeting FZD7.1, 2, 3, 2, 4, 2.1Department of Gynecology, The First Affiliated Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, People's Republic of China. .2Department of Gynecology, The First Affiliated Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, People's Republic of China.3Central Laboratory, China Medical University, Shenyang, 110001, People's Republic of China.4Department of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, 110001, People's Republic of China.AbstractMicroRNAs (miRNAs) are a class of small noncoding RNAs that play important roles in tumorigenesis and tumor progression through regulation of gene expression. Earlier, miR-142-3p was shown to decreased in c we explore the biological functional role of miR-142-3p and underlying mechanism in cervical cancer cells. We first detected the expression of miR-142-3p in six human cervical cancer cell lines and chose HeLa and SiHa cells for functional studies. By gain and loss of function experiments, we showed that overexpression of miR142-3p resulted in downregulation of Frizzled7 receptor (FZD7) and inhibited proliferation and invasion in HeLa and SiHa cells, whereas miR142-3p inhibitor-transfected cells showed reduced FZD7 expression and increased invasion capacity. In addition, we demonstrated that FZD7 was a direct target of miR-142-3p by dual luciferase assay and Western blot analysis. Overexpression of FZD7 expression was able to reverse the inhibitory effects induced by miR-142-3p. Taken together, miR-142-3p functions tumor suppressive effects in cell proliferation and invasion in cervical cancer cells, suggesting a potential therapeutic approach for cervical cancer.KEYWORDS: C FZD7; I P miR-142-3pPMID:
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External link. Please review our .Regulation of cell proliferation and migration by keratin19-induced nuclear import of early growth response-1 in breast cancer cells.
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2013 Aug 15;19(16):4335-46. doi: 10.32.CCR-12-3295. Epub
2013 Jul 5.Regulation of cell proliferation and migration by keratin19-induced nuclear import of early growth response-1 in breast cancer cells.1, , , , , , , , , .1Department of Life Science, Hanyang University, Seoul, Republic of Korea.AbstractPURPOSE: Keratin19 (KRT19) is the smallest known type I intermediate filament and is used as a marker for reverse transcriptase PCR-mediated detection of disseminated tumors. In this study, we investigated the functional analysis of KRT19 in human breast cancer.EXPERIMENTAL DESIGN: Using a short hairpin RNA system, we silenced KRT19 in breast cancer cells. KRT19 silencing was verified by Western blot analysis and immunocytochemistry. We further examined the effect of KRT19 silencing on breast cancer cells by cell proliferation, migration, invasion, colony formation assay, cell-cycle analysis, immunocytochemistry, immunohistochemistry, and mouse xenograft assay.RESULTS: Silencing of KRT19 resulted in increased cell proliferation, migration, invasion, and survival. These effects were mediated by upregulation of Akt signaling as a result of reduced PTEN mRNA expression. Silencing of KRT19 decreased the nuclear import of early growth response-1 (Egr1), a transcriptional factor for PTEN transcription, through reduced association between Egr1 and importin-7. We also confirmed that silencing of KRT19 increased tumor formation in a xenograft model.CONCLUSIONS: KRT19 is a potential tumor suppressor that negatively regulates Akt signaling through modulation of Egr1 nuclear localization.(C)2013 AACR.PMID:
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