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MicroRNA-138: A Diagnostic Biomarker and Therapeutic Target for the Aggressive Basal-like subtype of Breast Cancer

ABSTRACT: This study identifies miR-138 as a prognostic biomarker for basal breast carcinoma. Identification of differentially regulated genes upon miR-138 knockdown (AntagomiR-138) in basal breast cancer cell lines MDA-MB-231

ORGANISM(S): Homo sapiens

PROVIDER: GSE110659 | GEO | 2020/04/13

REPOSITORIES: GEO

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MicroRNA-138: A Diagnostic Biomarker and Therapeutic Target for the Aggressive Basal-like subtype of Breast Cancer

Project description:MicroRNA-138: A Diagnostic Biomarker and Therapeutic Target for the Aggressive Basal-like subtype of Breast Cancer

| PRJNA434203 | ENA

Over-expression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status

Project description:The tumor suppressor p53 is the most frequently mutated gene in human cancers, mutated in 25-30% of breast cancers. However, mutation rates differ according to breast cancer subtype, being more prevalent in aggressive estrogen receptor (ER) negative tumors, basal-like and HER2 amplified subtypes. This heterogeneity suggests that p53 may function differently across breast cancer subtypes. We used RNAi-mediated p53 knockdown (KD) and antagomir-mediated KD of microRNAs to study how gene expression and cellular response to p53 loss differ in luminal vs. basal-like breast cancer. As expected, p53 loss caused down regulation of established p53 targets (e.g. p21 and miR-34 family) and increased proliferation in both luminal and basal-like cell lines. However, some p53-dependent changes were subtype-specific, including expression of miR-134, miR-146a, and miR-181b. To study the cellular response to miR-146a upregulation in p53-impaired basal-like lines, antagomir knockdown of miR-146a was performed. KD of miR-146a caused decreased proliferation and increased apoptosis, effectively ablating the effects of p53 loss. Furthermore, we found that miR-146a upregulation decreased NF-kB expression and downregulated the NF-kB-dependent extrinsic apoptotic pathway (including TNF, FADD, and TRADD) and antagomir-mediated miR-146a KD restored expression of these components, suggesting a plausible mechanism for miR-146a-dependent cellular responses. These findings are relevant to human basal-like tumor progression in vivo, since miR-146a is highly expressed in p53-mutant basal-like breast cancers. These findings suggest that targeting miR-146a expression may have value for altering the aggressiveness of p53 mutant basal-like tumors. reference x sample

2014-06-30 | E-GEOD-52783 | biostudies-arrayexpress

Over-expression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status

2014-06-30 | GSE52783 | GEO

miR-138 controls interneuron function and short-term memory

Project description:Using a miR-138 loss-of-function mouse model, a role for the brain enriched microRNA miR-138 in the regulation of inhibitory synaptic transmission and short-term memory formation was shown.

2022-04-06 | GSE173982 | GEO

Inhibition of microRNA-138 enhances bone formation in multiple myeloma bone marrow niche

Project description:Myeloma bone disease is a devastating complication of multiple myeloma (MM) and is caused by dysregulation of bone remodeling processes in the bone marrow microenvironment. Previous studies showed that microRNA-138 (miR-138) is a negative regulator of osteogenic differentiation of mesenchymal stromal cells (MSCs) and that inhibiting its function enhances bone formation in vitro. In this study, we explored the role of miR-138 in myeloma bone disease and evaluated the potential of systemically delivered locked nucleic acid (LNA)-modified anti-miR-138 oligonucleotides in suppressing myeloma bone disease. We showed that expression of miR-138 was significantly increased in MSCs from MM patients (MM-MSCs) and myeloma cells compared to those from healthy subjects. Furthermore, inhibition of miR-138 resulted in enhanced osteogenic differentiation of MM-MSCs in vitro and increased number of endosteal osteoblastic lineage cells (OBCs) and bone formation rate in mouse models of myeloma bone disease. RNA sequencing of the OBCs identified TRPS1 and SULF2 as potential miR-138 targets that were de-repressed in anti-miR-138 treated mice. In summary, these data indicate that inhibition of miR-138 enhances bone formation in MM and that pharmacological inhibition of miR-138 could represent a new therapeutic strategy for treatment of myeloma bone disease.

2018-06-01 | GSE111651 | GEO

Identification of the downstream target genes of miR-138 in gastric cancer

Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.

2021-10-08 | GSE183654 | GEO

MicroRNA-138: A Pro-survival OncomiR for Glioma Stem Cells is Associated with Tumor Recurrence [mRNA]

Project description:We report the identification of microRNA-138 (miR-138), as a molecular signature of GSCs and demonstrate a vital role for miR-138 to promote growth and survival of bona fide tumor-initiating cells with self-renewal potential. Keywords: Expression profiling by array Total RNA from GSCs 5 days after transduction with lentivirus expressing anti-miR-138 or scrambled sequence was subjected to microarray analysis

2012-12-20 | E-GEOD-39487 | biostudies-arrayexpress

Identification of targets of miR-138 in Neuro-2a and 293T cells by RNAseq

Project description:We previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. We did not find other confirmed viral targets of miR-138. Therefore we conducted these RNAseq experiments (in combination with PAR-CLIP experiments whose results are uploaded separately) to identify host targets of miR-138 in two cell lines to explain the ICP0-independent effects on HSV-1 gene expression.

2020-04-27 | GSE127502 | GEO

MicroRNA-138: A Pro-survival OncomiR for Glioma Stem Cells is Associated with Tumor Recurrence [miRNA]

2012-12-20 | GSE39486 | GEO

Identification of viral and host targets of miR-138 by PAR-CLIP analysis of herpes simplex virus 2 infected 293T cells

Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.

2021-11-01 | GSE155402 | GEO

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