Exploring the involvement of Adathoda vasica in hypoxia axis at the molecular level
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PROVIDER: PRJNA658987 | ENA |
REPOSITORIES: ENA
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Project description:Hypoxic stress is a feature of rapidly growing thyroid tumors. Cancer progression is thought to be driven by reactive oxygen species (ROS) induced hypoxia adaptation. NADPH oxidases (NOXs), which produce ROS as their primary and sole function, has become of particular interest in thyroid malignancy. NOX4 was demonstrated to be upregulated in papillary thyroid cancers, functioning as a mitochondrial energetic sensor to modulate ATP levels, mediating overproduction of ROS induced by IL-δ, inversely correlating to thyroid differentiation. In this study, we analyzed hypoxia-treated BCPAP cells transfected with siRNA against NOX4. Results provides insight into the role of NOX4 in hypoxia adaptation.
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Project description:Rationale：Poor peri-implant osseointegration of dental implants in patients with type II diabetes has become a major clinical challenge in recent years. MSC (Mesenchymal stem cell)-derived exosomes may play an important role in peri-implant osseointegration, but the mechanism remains unclear. Enhancing the therapeutic effect of MSC-derived exosomes and exploring the potential mechanism can help provide a new therapeutic strategy to improve the clinical outcome of dental implant restorations in patients with type II diabetes. Methods：The exosomes derived from hypoxia (Hypo-exos) or normoxia (Nor-exos) preconditioned bone marrow mesenchymal stem cells (BMSCs) were co-cultured with BMSCs and human umbilical vein endothelial cells (HUVECs). The effect of exosomes on BMSCs cell proliferation was detected by CCK-8 assay and EdU assay, and the effect on angiogenesis ability of HUVECs was detected by wound healing assay, transwell migration assay, tube formation assay, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. A diabetic rat dental implant model was also established and the effect of exosomes on implant osseointegration was evaluated through micro-CT scanning and histological analysis. The differentially expressed miRNAs between Hypo-exos and Nor-exos were identified by high-throughput miRNA sequencing. Subsequently, the target genes and their roles in regulating angiogenesis were predicted and analyzed by bioinformatics analysis and dual luciferase reporter assay. Results：In vitro experiments indicated that hypoxia preconditioning could elevate exosome production and promote cell proliferation of BMSCs and angiogenesis of HUVECs. Moreover, Hypo-exos promoted peri-implant osteogenesis in rats with diabetes. Further investigation revealed the vital involvement of the miR-106b-5p/HIF-1α axis in promoting peri-implant osseointegration. Conclusion: Exosomes derived from hypoxia-preconditioned BMSCs could improve the peri-implant osseointegration in rats with diabetes by promoting cell proliferation and angiogenesis, and the miR-106b-5p/ HIF-1α axis could be the underlying mechanism.
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Project description:A hallmark of solid tumours is the development of hypoxic regions where rapidly growing transformed cells outstrip their blood supply. Tumour cells in these starved regions sense reduced levels of oxygen and switch on genes that help them to adapt, survive and continue growing. Since hypoxia is a key physiological difference between normal and cancer tissue, an opportunity exists to selectively kill tumour cells by exploiting the differences in protein expression between normal and hypoxic tumour tissue. However, a major challenge is to identify druggable hypoxia-induced proteins critical for tumour cell survival. This is especially important in cancers of unmet need where hypoxia gene signatures correlate with poor prognosis (for example, colorectal cancers). To identify new hypoxia-induced proteins, we performed SILAC-based proteomics on colorectal cancer cells exposed to normoxia and hypoxia. In this study, we identify a new hypoxia-activated GPCR signalling axis that enables colorectal tumour cells to survive the microenvironmental stress of hypoxia. Our findings uncover a previously unappreciated role for this GPCR-axis as a key regulator of the adaptive response to hypoxia and highlght an opportunity to exploit tumour-associated hypoxia for therapy.
2018-09-18 | PXD009971 | Pride
Project description:Hypoxia, a hallmark of most solid tumors, leads to aberrations in epigenetic modifications promoting malignant tumor phenotypes, including metastatic features and stem cell-like characteristics. Aberrant DNA methylation has been considered to play an essential role during tumor progression and tightly associate with tumor malignancy. However, the mechanism by which hypoxia alters DNA methylation to promote tumor malignancy remains poorly understood. Ten-eleven translocation 1-3 (TET1-3) proteins, which catalyze the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), play a critical role in the DNA demethylation that controls different biological processes. Here we demonstrate that the expression of TET1 and TET3 is closely associated with tumor hypoxia, tumor malignancy and poor prognosis of patients with breast cancer. Hypoxia results in deregulation of TET1 and TET3, leading to breast tumor initiating cell (BTIC) properties. Mechanically, hypoxia regulates expression of TET1 and TET3 via hypoxia-inducible factor-1a (HIF-1a), thereby resulting in 5hmC genome-wide changes, which in turn leads to the upregulation of TNFa expression and activation of its downstream p38-MAPK pathway. Importantly, signal transduction through the TET-TNFa-p38-MAPK signaling axis is required for the acquisition of BTIC characteristics and chemotherapy resistance, leading to more malignant tumor phenotypes. Inhibition of the hypoxia-TET-TNFα-p38-MAPK signaling pathway results in compromised BTIC properties and tumorigenicity in vitro and in vivo, suggesting a possible therapeutic strategy.
2015-10-05 | GSE60434 | GEO
Project description:Transcriptomic studies were undertaken to investigate the effect of hypoxia on kidney in early life to elucidate the genomic basis of renal injury and adaptation when oxygen is deprived. Fluorescently labeled, reverse-transcribed kidney RNA from 18 male and 18 female P2 mice, subjected for one, two or four weeks to normal atmospheric conditions (NAC) or to chronic constant (CCH) or intermittent (CIH) hypoxia were hybridized with 18 cDNA microarrays ("multiple yellow strategy", MYS). Expression level, stability, coordination and maturation of 1775 distinct genes were studied in each treatment-duration condition. Results: Both CIH and CCH change the expression level, stability and coordination of numerous genes that are involved in most major functional pathways. The fold change was significantly higher in female mice after one week of hypoxia and significantly higher in males after two and four weeks of hypoxia. Most solute carrier genes, including NHE1, are up-regulated and few down-regulated. There are genes coordinately expressed but others are much less so, with a remarkable overlap between the genes that are coexpressed in NAC and coregulated in CCH and CIH. Conclusion. Hypoxia is a major stress that alters the profile, stability and coordination of the kidney transcriptome in early life and slows down its maturation. Keywords: stress response
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