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MicroRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer (Human cell line)

ABSTRACT: MicroRNA deregulation is frequent in human colorectal cancers (CRCs) but little is known to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b over-expression is triggered in mouse and humans by APC loss, PTEN/PI3K pathway deregulation and by SRC over-expression and promotes tumor transformation and progression. We show that miR-135b up-regulation is common to sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth controlling genes involved in proliferation, invasion and apoptosis. We identify miR-135b as a key down-steam effector of oncogenic pathways and a potential novel target for CRC patientM-bM-^@M-^Ys treatment. RNA was extracted using trizol from normal human colon cell lines comparing scrambled with miR-135b oligos transfected cells

ORGANISM(S): Homo sapiens

SUBMITTER: Luciano Cascione

PROVIDER: E-GEOD-54163 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer (mouse)

Project description:MicroRNA deregulation is frequent in human colorectal cancers (CRCs) but little is known to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b over-expression is triggered in mouse and humans by APC loss, PTEN/PI3K pathway deregulation and by SRC over-expression and promotes tumor transformation and progression. We show that miR-135b up-regulation is common to sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth controlling genes involved in proliferation, invasion and apoptosis. We identify miR-135b as a key down-steam effector of oncogenic pathways and a potential novel target for CRC patient’s treatment. RNA was extracted from fresh frozen tissues from tumours from APC;CpC and AOM/DSS mice and normal matched tissues

2014-01-17 | E-GEOD-54177 | biostudies-arrayexpress

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer (mouse)

2014-01-17 | GSE54177 | GEO

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer (Human cell line)

2014-01-17 | GSE54163 | GEO

The effect of miRNA-135b overexpression on the gene expression profile of LNCaP cells

Project description:MicroRNAs (miRNAs) regulate a wide range of cellular signaling pathways and biological processes in both physiological and pathological states such as cancer. We have previously identified miR-135b as a direct regulator of androgen receptor (AR) protein level in prostate cancer (PCa). We wanted to further explore the relationship of miR-135b to hormonal receptors, particularly estrogen receptor α (ERα). Here we show that miR-135b expression inversely correlates with ER protein in two independent breast cancer (BCa) patient cohorts (101 and 1302 samples) and with AR protein in 47 PCa patient samples. We identify ERα as a novel miR-135b target by demonstrating miR-135b binding to the 3’UTR of the ERα and decreased ERα protein and mRNA level in breast cancer cells upon miR-135b overexpression. miR-135b inhibits proliferation of hormone receptor positive cancer cell lines as shown by overexpression in ERα-positive BCa cells (MCF-7) and AR-positive PCa cells (LNCaP, 22Rv1) when grown in 2D. To identify other genes regulated by miR-135b we performed gene expression studies and found a potential link to the hypoxia-inducible factor-1α (HIF1α) pathway. We show that miR-135b influences the protein level of the inhibitor for hypoxia-inducible factor-1 (HIF1AN), which also demonstrated an inverse correlation with miR-135b in a cohort of breast tumor samples. Taken together, our study demonstrates that miR-135b regulates ERα, AR and HIF1AN protein levels and proliferation in ERα -positive breast and AR-positive-prostate cancer cells.

2015-04-21 | GSE57820 | GEO

miR-135b expression effect on myxoid liposarcoma cell line

Project description:miR-135b expression is higher in myxoid liposarcoma cell lines than in adipose-derived mesenchymal cell line, as well as in myxoid liposarcoma tumors than in adjacent normal prostate tissues.To further investigate the molecular mechanisms regulated by miR-135b, we performed mRNA microarray analysis of cell cultures from myxoid liposarcoma cell line after transfections with miR-135b mimic or negative control.

2017-02-09 | GSE73347 | GEO

miRNA 135b regulation of inflammation

2013-01-31 | GSE43681 | GEO

miRNA 135b regulation of inflammation

Project description:RT-PCR analysis of inflammatory cytokines and receptors in pEGP-miR-135b over-expressing cells compard to controls (pEGP-miR-null) using pathway-specific PCR arrays for the evaluation of mouse inflammatory cytokines and receptors (#PAMM-011D). qPCR array gene expression profiling. This experiment examined the transcriptional response of NIH3T3 cells over-expressing pEGP-miR-135b. Total RNA (n = 3 per group) was used with SABiosciences pathway-specific PCR arrays for inflammatory cytokines and receptors (#PAMM-011D).

2013-01-31 | E-GEOD-43681 | biostudies-arrayexpress

miRNA 135b regulation by Il1r1 during inflammation

2013-01-31 | GSE43683 | GEO

miRNA 135b regulation by Il1r1 during inflammation

Project description:RT-PCR analysis of inflammatory cytokines and receptors following Il1alpha treatment of pEGP-miR-135b over-expressing cells compard to controls (pEGP-miR-null) using pathway-specific PCR arrays for the evaluation of mouse inflammatory cytokines and receptors (#PAMM-011D). qPCR array gene expression profiling. This experiment examined the transcriptional response of NIH3T3 cells over-expressing pEGP-miR-135b following IL1alpha treatment. Total RNA (n = 3 per group) was used with SABiosciences pathway-specific PCR arrays for inflammatory cytokines and receptors (#PAMM-011D).

2013-01-31 | E-GEOD-43683 | biostudies-arrayexpress

miR-135b exerts metastatic activity in the ErbB2 driven mammary carcinogenesis

Project description:In view of the roles played by miRNAs in cancer progression, we performed a microarray analysis aimed at identifying miR-135b target genes in breast cancer cells. Detection of transcripts affected by silencing of mir-135b was done using a time course at 24, 48 and 72 h both transfecting cell with mir-135b specific miRIDIAN microRNA Hairpin Inhibitor or miRIDIAN microRNA Hairpin Inhibitor negative control. Each experimental condition was repeated three times and analysed on on MOUSEREF-8 V2 Illumina bead chips. Genome studio was used to generate raw intensity signal without normalization. Data log2 transformation and loess normalization was performed with oneChannelGUI. Data were filtered using an IQR filter (i.e. only genes characterized by an IQR > 0.25, were retained for further analysis). Detection of differentially expressed transcripts was also performed with oneChannelGUI, using masigpro package with default parameters. Data were visualized by hierarchical clustering, as log2 ratio between anti-miR135b and the negative control using TMEV software. The subset of transcripts characterized by an increase in expression as consequence of a reduction of expression of miR135b were selected. MicroRNA target data for mir135b were retrieved from miranda database (microRNAsmiranda.mouse_predictions_S_C_aug2010.txt, http://www.microrna.org/microrna/home.do). Miranda data and transcripts increasing their expression upon silencing of miR135b were intersected to find the genes in common. Detection of transcripts affected by silencing of mir-135b was done using a time course at 24, 48 and 72 h both transfecting cell with mir-135b specific miRIDIAN microRNA Hairpin Inhibitor or miRIDIAN microRNA Hairpin Inhibitor negative control.

2013-12-01 | E-GEOD-28949 | biostudies-arrayexpress

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