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Signature of MicroRNAs with Impact on Angiogenesis in Non-Small Cell Lung Cancer

ABSTRACT: Angiogenesis is regarded as a hallmark in cancer development, and anti-angiogenic treatment is presently used in non-small cell lung cancer (NSCLC) patients. MicroRNAs (miRs) are small non-coding, endogenous, single stranded RNAs that regulate gene expression. As miRs are relatively stabile and measurable in both tissue and serum, they are potential prognostic and predictive markers. In this study we aimed to identify significant altered miRs related to angiogenesis in NSCLC

ORGANISM(S): Merkel cell polyomavirus Human gammaherpesvirus 8 Mus musculus Rattus norvegicus JC polyomavirus Betapolyomavirus macacae Homo sapiens Murid gammaherpesvirus 4 Human immunodeficiency virus 1 Human betaherpesvirus 5 Human alphaherpesvirus 2 Betapolyomavirus hominis Human alphaherpesvirus 1 human gammaherpesvirus 4 Mus musculus cytomegalovirus 2

PROVIDER: GSE27705 | GEO | 2011/03/08

SECONDARY ACCESSION(S): PRJNA138125

REPOSITORIES: GEO

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Signature of MicroRNAs with Impact on Angiogenesis in Non-Small Cell Lung Cancer

Project description:Angiogenesis is regarded as a hallmark in cancer development, and anti-angiogenic treatment is presently used in non-small cell lung cancer (NSCLC) patients. MicroRNAs (miRs) are small non-coding, endogenous, single stranded RNAs that regulate gene expression. As miRs are relatively stabile and measurable in both tissue and serum, they are potential prognostic and predictive markers. In this study we aimed to identify significant altered miRs related to angiogenesis in NSCLC From a large cohort of 335 NSCLC patients, paraffin-embedded samples from 10 patients with a short disease specific survival (DSS), 10 with a long DSS and 10 normal controls were analyzed.

2011-03-08 | E-GEOD-27705 | biostudies-arrayexpress

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

Project description:Anlotinib, a multitarget agent a multi-target agent that inhibits tumor proliferation and angiogenesis, has been demonstrated to be effective for non-small cell lung cancer (NSCLC) at third-line or over third-line. However, the underlying mechanisms of anlotinib acquired-resistance is still unclear. Here we performed chromatin accessibility profiling on anlotinib-resistant NCI-H1975 and wild-type NCI-H1975. By integrating with transcriptome analysis, we found that anlotinib resistance was due to increased angiogenic capacity, and revealed that TFAP2A was involved in anlotinib resistance. Next, TFAP2A was knock-down in anlotinib-resistant cells and RNAseq was performed to see down-regulated genes with TFAP2A KD.

2020-11-09 | GSE142031 | GEO

Cancer associated fibroblast-derived WNT2 increases tumor angiogenesis in colon cancer

Project description:WNT2 is important for placenta vascularization and acts as a pro-angiogenic factor for liver and other endothelial cells (ECs). WNT2 induction has been shown in many carcinomas and is associated with tumor progression. In colorectal cancer (CRC) WNT2 is selectively elevated in cancer associated fibroblasts (CAFs), leading to increased invasion and metastasis. However, if there is a role for WNT2 in colon cancer angiogenesis has not been addressed so far. Here, we demonstrate that WNT2 enhances EC migration and invasion, while it induces ß catenin dependent signaling in only a small subset of HUVECs. We show that siRNA-mediated knockdown of WNT2 in CAFs reduced the growth of vessel-like structures significantly in a co-culture assay, while the overexpression of WNT2 in skin fibroblasts otherwise being devoid of WNT2 led to increased angiogenesis in vitro. In a xenograft model, overexpression of WNT2 in HCT116 led to enhanced tumor volume and vessel density. Moreover, WNT2 expression correlates with vessel markers in human CRC. Secretome profiling of CAFs revealed that proteins related to angiogenesis and extracellular matrix (ECM) remodeling are regulated by WNT2. Thus, stroma-derived WNT2 positively affects angiogenesis in CRC by shifting the balance towards pro-angiogenic signals.

2020-05-26 | PXD014019 | Pride

DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small cell lung cancer

Project description:DUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To understand more about the cellular responses regulated by DUSP1 in NSCLC cells, we interfered DUSP1 expression in the NSCLC cell line H460 and studied the changes in gene expression differentially regulated by this phosphatase. Keywords: Expression profiling by array in cells with genetic modification The human non small lung cancer cell line H460 used in this study was from ATCC (American Type Culture Collection). The cell line was maintained in RPMI (Gibco, Invitrogen) supplemented with 10% bovine serum and transfected by Lipofectamine Plus Reagent from Life Technologies as directed by the manufacturer. The DUSP1 pSuperRetro-derived vectors were constructed as described (Chattoppadhyay et al., 2006). Clones expressing siRNA for DUSP1 were selected for their ability to grow in the presence of puromycin and kept for selection. Stable transfection was confirmed by Western blotting. RNA was extracted and quality control was checked before hybridization on Affymetrix microarrays.

2010-12-09 | E-GEOD-19592 | biostudies-arrayexpress

Loss of apelin blocks the emergence of sprouting angiogenesis in experimental tumors

Project description:Angiogenesis-inhibitor (AI) drugs targeting vascular endothelial growth factor (VEGF) signalling to the endothelial cell (EC) are used to treat various cancers types. However, primary or secondary resistance to therapy is common. Clinical and pre-clinical studies suggest that other alternative pro-angiogenic factors are up-regulated after VEGF-pathway inhibition. Therefore, identification alternative pro-angiogenic pathway(s) is critical for the development of more effective anti-angiogenic therapy. Here we study the role of apelin as a pro-angiogenic G-protein coupled receptor (GPCR) ligand in tumor growth and angiogenesis. We applied single-cell RNA-sequencing to Mouse Lewis lung carcinoma (LLC1) or B16F10 mouse melanoma cell lines (1 X 106) implanted subcutaneously into the flanks of 12 weeks old Apln-/y or littermate control mice in combination with sunitinib or control (vehicle) treatment. We found apelin loss reduced angiogenic sprouting and tip cell marker gene expression in comparison to the sunitinib-alone treated mice and prevented EC tip cell differentiation.

2023-04-06 | E-MTAB-11663 | biostudies-arrayexpress

Pigment epithelium derived factor (PEDF): a novel trophoblast derived factor limiting feto-placental angiogenesis in late pregnancy

Project description:We hypothesized that the trophoblast secretes anti-angiogenic factors, which increase in late pregnancy to limit angiogenesis. Therefore, we determined the paracrine effect of primary human trophoblasts from early versus late pregnancy on the angiogenic potential of isolated feto-placental endothelial cells. We found that the expression and secretion of anti-angiogenic factors differs in early vs late pregnancy, and differentially affects feto-placental angiogenesis.

2017-01-01 | GSE69086 | GEO

Identification of specifically activated angiogenic molecules in HMGB-1-induced angiogenesis

Project description:High-mobility group box-1 (HMGB-1), a nonhistone chromosomal protein, is expressed in almost all types of cells with nucleus, and dysregulation of its expression correlates with pathological conditions such as inflammatory diseases, ischemia and cancers. Some of these conditions accompany abnormal angiogenesis induced by HMGB-1 mediated activation of downstream signaling pathways. So far, the underlying mechanism by which HMGB-1 induces angiogenesis remains largely unknown. In this study, we performed time-dependent gene expression microarray in endothelial cells (ECs) after HMGB-1 or VEGF treatment. By pathway analysis using each gene set up-regulated by HMGB-1 or VEGF, we found that most of HMGB-1 induced angiogenic pathways were also commonly activated by VEGF, while activation time and gene sets belonging to the pathways were different. In addition, HMGB-1 up-regulated some VEGFR signaling related conventional angiogenic factors including EGR1 and importantly, novel angiogenic factors such as ABL2, CEACAM1, KIT and VIPR1 which have been reported to independently promote angiogenesis in physiological and pathological conditions. Our gene expression profiling suggests that HMGB-1 is capable of independently inducing angiogenesis through activation of HMGB-1 specific angiogenic factors and also functions as an accelerator for VEGF mediated conventional angiogenesis according to physiological and pathological condition.

2017-12-29 | GSE100404 | GEO

Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4+ endothelial cells

Project description:Exercise is a powerful driver of physiological angiogenesis during adulthood, but the mechanisms of exercise-induced vascular expansion are poorly understood. We explored endothelial heterogeneity in skeletal muscle and identified two capillary muscle endothelial cells (mEC) populations which are characterized by differential expression of ATF3/4. Spatial mapping showed that ATF3/4 + mECs are enriched in red oxidative muscle areas while ATF3/4 low ECs lie adjacent to white glycolytic fibers. In vitro and in vivo experiments revealed that red ATF3/4 + mECs are more angiogenic when compared to white ATF3/4 low mECs. Mechanistically, ATF3/4 in mECs control genes involved in amino acid uptake and metabolism and metabolically prime red (ATF3/4 + ) mECs for angiogenesis. As a consequence, supplementation of non-essential amino acids and overexpression of ATF4 increased proliferation of white mECs. Finally, deleting Atf4 in ECs impaired exercise-induced angiogenesis. Our findings illustrate that spatial metabolic angiodiversity determines the angiogenic potential of muscle ECs.

2021-06-15 | GSE174785 | GEO

Different Preference of Degradome in Invasion versus Angiogenesis

Project description:We hypothesized altered expression of Proteases in calls capable of physiological invasion vs angiogenesis. We analyzed trophoblasts isolated from first trimester placenta that are invasive, and placental endothelial cells, that gave a high angiogenic potential. We found different expression levels of most proteases. We found that the expression of proteases differes in cells performing invasion vs cells performing angiogenesis.

2015-05-20 | GSE59126 | GEO

Angiogenesis study of Gd@C82(OH)22 nanoparticle

Project description:we report a novel nanomedicine (Gd@C82(OH)22 ) effectively inhibit human breast tumor growth by antiangiogenesis in vivo. To further identify which angiogenic factor(s) were affected on mRNA level, the "RT² Profiler™ PCR Array Mouse Angiogenesis (APMM-024, SuperArray Bioscience Corporation)" was used. Keywords: nanomedicine, Gd@C82(OH)22, angiogenesis, MCF-7, breast cancer

2009-04-01 | GSE7861 | GEO

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