MiRNA expression profiles of BLID shRNA vs. control (Scramble) shRNA transduced breast cancer cells
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE295734 | GEO | 2025/06/11
REPOSITORIES: GEO
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Project description:Downregulation of BLID in breast cancer has been correlated with poor disease-free survival and overall survival. We used RNA arrays to study the effects of BLID knockdown on gene expression profiles and to identify downstream effectors of BLID in breast cancer cells.
2025-06-11 | GSE295735 | GEO
Project description:miRNA expression profiles of BLID shRNA vs. control (Scramble) shRNA transduced breast cancer cells
| PRJNA1258933 | ENA
Project description:RNA expression profiles of BLID shRNA vs. control (scramble) shRNA transduced breast cancer cells
| PRJNA1258932 | ENA
Project description:MicroRNA (miRNA/miR) miR526b and miR655 overexpressed tumor cell-free secretions promote breast cancer phenotypes in the tumor microenvironment (TME). However, the mechanisms of miRNA regulating TME have never been investigated. With mass spectrometry analysis of MCF7-miRNA-overexpressed versus miRNA-low MCF7-Mock tumor cell secretomes, we identified 34 novel secretory proteins coded by eight genes YWHAB, TXNDC12, MYL6B, SFN, FN1, PSMB6, PRDX4, and PEA15 those are differentially regulated. We used bioinformatic tools and systems biology approaches to identify these markers’ role in breast cancer. Gene ontology analysis showed that the top functions are related to apoptosis, oxidative stress, membrane transport, and motility, supporting miRNA-induced phenotypes. These secretory markers expression is high in breast tumors, and a strong positive correlation exists between upregulated markers’ mRNA expressions with miRNA cluster expression in luminal A breast tumors. Gene expression of secretome markers is higher in tumor tissues compared to normal samples, and immunohistochemistry data supported gene expression data. Moreover, both up and downregulated marker expressions are associated with breast cancer patient survival. miRNA regulates these marker protein expressions by targeting transcription factors of these genes. Premature miRNA (pri-miR526b and pri-miR655) are established breast cancer blood biomarkers. Here we report novel secretory markers upregulated by miR526b and miR655 (YWHAB, MYL6B, PSMB6, and PEA15) are significantly upregulated in breast cancer patients’ plasma, and are potential breast cancer biomarkers.
2023-05-10 | PXD031771 | Pride
Project description:Obscurins (~70-870kDa), encoded by the single OBSCN gene, are cytoskeletal proteins originally identified in striated muscles with structural and regulatory roles. Recently, analysis of 13,023 genes in breast and colorectal cancers identified OBSCN as one of the most frequently mutated genes, implicating it in cancer formation. Herein, we studied the expression profile of obscurins in breast, colon and skin cancer cell lines, and their involvement in cell survival. Immunoblot analysis demonstrated significant reduction of obscurins in cancer cells, resulting from decreased mRNA levels and/or the presence of mutant transcripts. In normal epithelium, obscurins localize in cytoplasmic puncta, the cell membrane and the nucleus. Accordingly, subcellular fractionation demonstrated the presence of two novel nuclear isoforms of ~110 and ~120kDa. Non-tumorigenic MCF10A breast epithelial cells stably transduced with shRNAs targeting giant obscurins exhibited increased viability (~30%) and reduced apoptosis (~20%) following exposure to the DNA damaging agent, etoposide. cDNA microarrays followed by Gene Ontology profiling indicated a substantial number of transcripts related to apoptosis and survival are differentially regulated upon obscurin knock-down. Quantitative RT-PCR further indicated that the anti-apoptotic genes BAG-4 and HAX-1 were up-regulated (1.5 and 1.4 fold, respectively), whereas initiator caspase-9 and death caspase-3 transcripts were down-regulated (0.8 and 0.6 fold, respectively). Our findings are the first to pinpoint critical roles for obscurins in cancer development by contributing to the regulation of cell survival. Two-condition experiment: control shRNA- vs. obscurin shRNA-expressing MCF10A cells exposed to 150 uM etoposide. 3 independent replicates per condition.
2012-02-02 | E-GEOD-35494 | biostudies-arrayexpress
Project description:Obscurins (~70-870kDa), encoded by the single OBSCN gene, are cytoskeletal proteins originally identified in striated muscles with structural and regulatory roles. Recently, analysis of 13,023 genes in breast and colorectal cancers identified OBSCN as one of the most frequently mutated genes, implicating it in cancer formation. Herein, we studied the expression profile of obscurins in breast, colon and skin cancer cell lines, and their involvement in cell survival. Immunoblot analysis demonstrated significant reduction of obscurins in cancer cells, resulting from decreased mRNA levels and/or the presence of mutant transcripts. In normal epithelium, obscurins localize in cytoplasmic puncta, the cell membrane and the nucleus. Accordingly, subcellular fractionation demonstrated the presence of two novel nuclear isoforms of ~110 and ~120kDa. Non-tumorigenic MCF10A breast epithelial cells stably transduced with shRNAs targeting giant obscurins exhibited increased viability (~30%) and reduced apoptosis (~20%) following exposure to the DNA damaging agent, etoposide. cDNA microarrays followed by Gene Ontology profiling indicated a substantial number of transcripts related to apoptosis and survival are differentially regulated upon obscurin knock-down. Quantitative RT-PCR further indicated that the anti-apoptotic genes BAG-4 and HAX-1 were up-regulated (1.5 and 1.4 fold, respectively), whereas initiator caspase-9 and death caspase-3 transcripts were down-regulated (0.8 and 0.6 fold, respectively). Our findings are the first to pinpoint critical roles for obscurins in cancer development by contributing to the regulation of cell survival.
2012-02-02 | GSE35494 | GEO
Project description:We used MYOSIN10 shRNA to stably silence the expression of endogenous MYOSIN10 in Breast cancer cell MDA-MB-231. To investigate the inner change of cells with silenced MYOSIN10, we conducted a genome-wide screening for all potential genes affected by MYOSIN10 shRNA using Affymetrix Human Genome U133 plus 2.0 array. We showed genes affected by MYOSIN10 knockdown in breast cancer cell MDA-MB-231
2020-12-31 | GSE52828 | GEO
Project description:We reported glutathione peroxidase-1 (GPx1) was negatively associated with overall survival in pancreatic ductal adenocarcinoma patients. Silencing GPx1 in pancreatic cancer cells showed epithelial–mesenchymal transition phenotype and increased chemoresistance to gemcitabine in vitro and in vivo. Next, to search for a putative molecular mechanism, we used a high-throughput gene expression profiling array in scramble-shRNA and GPx1-shRNA pancreatic cancer cells (MiaPaCa-2). This study provides the differentially expressed genes and altered signaling pathways towards characterization of gemcitabine resistance cell populations.
2020-10-10 | GSE104962 | GEO
Project description:Previously, we have confirmed the tumor suppressive role of Estrogen Related Receptor β (ERRβ) in breast cancer by modulation of ER transcriptional activities on Breast Cancer Amplified Sequence 2 (BCAS2) and Follistatin(FST).In the mentioned study, we proved downregulation of Cyclin D1 by BCAS2.In the previous report, we have also proved downregulation of FST by BCAS2 through inhibition of β-catenin/TCF-4 complex recruitment on FST promoter. Interestingly, Cyclin D1 induction by FST has been also reported by a different group.Recently, Cyclin D1 expression has been found to be associated with DICER1 induction. Hence it may be speculated, that a part of miRNA population, which involves Dicer for processing, is regulated by BCAS2. And it is also possible, that FST may oppose the effect of BCAS2 on those Dicer-processed miRNAs.This Dicer-regulation by Cyclin D1was reported in Luminal A type of breast cancer. Hence, we chose MCF-7 breast cancer cells for miRNA profiling post knocking down BCAS2 and FST.
2017-10-31 | GSE89390 | GEO
Project description:DCD is a gene amplified and overexpressed in a subset of breast tumors acting as a growth and survival factor. Patients with DCD-positive breast cancer have worse prognostic features. To investigate the role of DCD in breast tumorigenesis, we analyzed the consequences of its downregulation in human breast cancer cell lines using three specific shRNA lentivirus vectors. Genes up- and down-regulated by DCD were identified using Affymetrix microarray and analyzed by MetaCore Platform. We found that loss of DCD expression led to reduced cell proliferation, resistance to apoptosis, and suppressed tumorigenesis in immunodeficient mice. Network analysis of gene expression data revealed perturbed ERBB signaling following DCD shRNA expression including changes in the expression of ERBB receptors and their ligands. These findings imply that DCD promotes breast tumorigenesis via modulating the activity of the ERBB signaling pathways. As ERBB signaling is also important for neural survival, HER2+ breast tumors may highjack DCD’s neural survival-promoting functions to promote tumorigenesis.
2015-08-12 | GSE57578 | GEO