Galectin-9 suppresses tumor growth of colon cancer in vitro and in vivo [in vitro CW]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE163592 | GEO | 2021/05/05
REPOSITORIES: GEO
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Project description:We examined the ability of Gal-9 to inhibit cell proliferation via apoptosis, and the effects of Gal-9 on cell cycle-related molecules in various human colon and colorectal cancer cell lines. In addition, Gal-9-mediated changes of activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal-9-induced miRNA expression profiles. We also elucidated if Gal-9 inhibited tumor growth murine in vivo model.
2021-05-05 | GSE163599 | GEO
Project description:We examined the ability of Gal-9 to inhibit cell proliferation via apoptosis, and the effects of Gal-9 on cell cycle-related molecules in various human colon and colorectal cancer cell lines. In addition, Gal-9-mediated changes of activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal-9-induced miRNA expression profiles. We also elucidated if Gal-9 inhibited tumor growth murine in vivo model.
2021-05-05 | GSE163789 | GEO
Project description:We examined the ability of Gal-9 to inhibit cell proliferation via apoptosis, and the effects of Gal-9 on cell cycle-related molecules in various human colon and colorectal cancer cell lines. In addition, Gal-9-mediated changes of activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal-9-induced miRNA expression profiles. We also elucidated if Gal-9 inhibited tumor growth murine in vivo model.
2021-05-05 | GSE163786 | GEO
Project description:We examined the ability of Gal-9 to inhibit cell proliferation via apoptosis, and the effects of Gal-9 on cell cycle-related molecules in various human colon and colorectal cancer cell lines. In addition, Gal-9-mediated changes of activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal-9-induced miRNA expression profiles. We also elucidated if Gal-9 inhibited tumor growth murine in vivo model.
2021-05-05 | GSE163782 | GEO
Project description:We examined the ability of Gal-9 to inhibit cell proliferation via apoptosis, and the effects of Gal-9 on cell cycle-related molecules in various human colon and colorectal cancer cell lines. In addition, Gal-9-mediated changes of activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal-9-induced miRNA expression profiles. We also elucidated if Gal-9 inhibited tumor growth murine in vivo model.
2021-05-05 | GSE163606 | GEO
Project description:Aortic stenosis (AS) is a degenerative valve disease characterized by active remodelling of valve leaflets. The main hallmarks of stenotic aortic valves (AVs) include fibrosis, inflammation, osteogenesis and angiogenesis. Men and women develop these mechanisms differently. Galectin-3 (Gal-3) is a pro-inflammatory and pro-osteogenic lectin with a prominent role in the progression of AS. In this work, we aim to analyze potential sex-differences in the impact of Gal-3 in AS. 226 patients (61.50% men) with severe AS undergoing surgical valve replacement were recruited. In AVs, Gal-3 expression and its relationship with inflammatory, osteogenic and angiogenic markers was assessed. Valve interstitial cells (VIC) derived from AV tissue were primary cultured to perform in vitro experiments. Proteomic analysis revealed that Gal-3 is over-expressed in VICs of male AS patients. Gal-3 secretion also showed to be higher in men’s VICs as compared to women. In human AV tissue, Gal-3 protein levels were significantly higher in men, with stronger immunostaining in VICs with myofibroblastic phenotype and valve endothelial cells. Gal-3 levels in AVs were positively correlated with inflammatory markers in both sexes. Gal-3 expression was also positively correlated with osteogenic markers mainly in men’s AV, and with angiogenic molecules only in this sex.
2024-05-31 | PXD042586 | JPOST Repository
Project description:Galectin-1 (Gal-1) is a lectin, involved in several processes related to cancer, including immunosuppression, angiogenesis, hypoxia, and metastases. Actually, the Gal-1 expression profile in multiple myeloma (MM) and its pathophysiological role in MM–induced angiogenesis and tumoral growth is unknown. Firstly, we found that Gal-1 was expressed by malignant plasma cells in MM patients and that its expression was up-regulated upon hypoxic treatment (1% of O2). Moreover the stable knock-down of Hypoxia Inducible Factor-1α (HIF-1α) in MM cells significantly downregulated Gal-1 expression. Thereafter, we performed Gal-1 inhibition by lentivirus shRNA anti-Gal-1 in human myeloma cell lines (HMCLs) showing that its suppression did not affect cell proliferation and survival but modified their transcriptional profiles either in hypoxia or hypoxia condition. Interestingly pro-angiogenic genes including MMP9 and CCL2 were downregulated and those anti-angiogenic SEMA3A and CXCL10 were up-regulated by Gal-1 inhibition in MM cells. Data were also validated by Real time PCR and at protein level. Consistently we found that Gal-1 suppression in MM cells significantly decreased their pro-angiogenic proprieties by an in vitro assay. These evidences were confirmed in mice injected either subcutaneously or intratibially with HMCLs carrying a stable infection with shRNA anti-inhibition of Gal-1 or with the control vector cell line. Gal-1 suppression in both models showed a significant reduction in the tumoral burden and microvascular density compared to the control mice. Moreover, Gal-1 suppression induced smaller lytic lesions on x-ray in the intratibially model. Overall, our data indicate that Gal-1 is a new potential therapeutic target in MM.
2016-11-27 | GSE75101 | GEO
Project description:Background: Retinal neovascularization (RNV) is a leading cause of blindness worldwide. Long non-coding RNA (lncRNA) and competing endogenous RNA (ceRNA) regulatory networks play vital roles in angiogenesis. The RNA-binding protein galectin-1 (Gal-1) participates in pathological RNV in oxygen-induced retinopathy mouse models. However, the molecular associations between Gal-1 and lncRNAs remain unclear. Herein, we aimed to explore the potential mechanism of action of Gal-1 as an RNA-binding protein. Results: A comprehensive network of Gal-1, ceRNAs, and neovascularization-related genes was constructed based on transcriptome chip data and bioinformatics analysis of human retinal microvascular endothelial cells. We also conducted functional enrichment and pathway enrichment analyses. Fourteen lncRNAs, twenty-nine miRNAs, and eleven differentially expressed angiogenic genes were included in the Gal-1/ceRNA network. WT1-AS, LINC01140, and LUCAT1 were situated at the center of the network. Additionally, several key angiogenic genes, such as apelin, angiomotin, and C-X-C motif chemokine ligand 10, were found to potentionally interact with Gal-1 via the ceRNA axis. Furthermore, Gal-1 may be involved in regulating biological processes related to chemotaxis, chemokine-mediated signaling, the immune response, and the inflammatory response. Conclusions: The Gal-1/ceRNA axis identified in this study may play a vital role in RNV. This study provides a foundation for the continued exploration of therapeutic targets and biomarkers associated with RNV.
2023-06-21 | GSE221037 | GEO
Project description:Identification of interactors is a major attempt in cell biology. Not only protein-protein but also protein-carbohydrate interactions are of high relevance for signal transduction in biological systems. Here we aim to identify novel interacting binding partners for the β-galactoside-binding proteins Galectin-1 (Gal-1) and Galectin-3 (Gal-3) in context of the eye disease proliferative vitreoretinopathy (PVR). PVR is one of the most common failures after retinal detachment surgeries and is characterized by the migration, adhesion and epithelial-to-mesenchymal transition (EMT) of retinal pigment epithelial cells (RPE) and the subsequent formation of sub- and epiretinal fibrocellular membranes. Gal-1 and Gal-3 bind in a dose- and carbohydrate-dependent manner to mesenchymal RPE cells and inhibit cellular processes like attachment and spreading. Yet knowledge about glycan-dependent interactors of Gal-1 and Gal-3 on RPE cells is very limited, although this is a prerequisite to unravel the influence of galectins on distinct cellular processes in RPE cells. In this approach, we identified by galectin pull-down experiments and quantitative proteomic screening 131 Galectin-3 and 15 Galectin-1 interactors. They mainly play a role in multiple binding processes and are mostly membrane proteins. Here we focused on two novel identified interactors of Gal-1 and Gal-3 in the context of PVR: the low-density lipoprotein receptor LRP1 and the platelet-derived growth factor receptor beta PDGFRB. We observed crosslinking and lattice formation of exogenous Gal-1 and Gal-3 with LRP1/PDGFRB and ITGB1 on the cell surface of human RPE cells. Weaker binding of Gal-1 and Gal-3 on these interactors and no lattice formation on the cell surface was seen, when complex-type-N-glycosylation was inhibited by treatment of the cells with Kifunensine. In conclusion, the identified specific glycoprotein ligands for Gal-1 and Gal-3 give us new insights in the highly specific binding of galectins to dedifferentiated RPE cells and the resulting prevention of PVR-associated cellular events.
2017-06-06 | PXD005461 | Pride
Project description:Active immunotherapy is a promising strategy for anti-angiogenic cancer therapy. Recently, we have reported that a vaccine using human umbilical vein endothelial cells (HUVECs) induced specific anti-endothelial immune responses in the most of immunized patients, and resulted in tumor regression in some patients with recurrent malignant brain tumors, whereas not in colorectal cancer patients. In this study, we hypothesized that non-hypoxic perivascular tumor associated macrophages (TAMs) in colorectal cancer, but not in glioblastoma, might negatively alter the therapeutic efficacy of anti-angiogenic active immunotherapy. To test this hypothesis, we examined global gene expression profiles of non-hypoxic macrophages stimulated in vitro by soluble factors released from tumor cells of human glioblastoma U-87MG (‘brain TAMs’) or colorectal adenocarcinoma HT-29 (‘colon TAMs’).
2012-04-01 | GSE18804 | GEO