Exposure to the olfactory receptor 51E1 agonist nonanoic acid alters small intestinal neuroendocrine tumor phenotype
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE216067 | GEO | 2022/10/21
REPOSITORIES: GEO
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Project description:Small intestinal neuroendocrine tumors (SI-NETs) arise from serotonin-producing enterochromaffin cells. SI-NETs are often well-differentiated tumors and most patients have regional or distant metastases at initial presentation. MicroRNAs (miRs) are post-transcriptional regulators which are important in diverse biological processes and can function as tumor suppressor genes or oncogenes. This study aims to identify an exclusive SI-NETs miR profile that may have a critical role in development, diagnosis, prognosis and progression of these malignancies. Five human NET cell lines, one octreotide-treated CNDT2.5 cells, one microdissected normal enterochromaffin cells, three snap-frozen normal ileum specimens and 15 SI-NET specimens at different stage of malignancy, five primary tumors, five mesentery metastases and five liver metastases, were included in this study. Total RNA was hybridized onto Affymetrix GeneChipM-BM-. miR arrays for genome-wide profiling. Array data summarization, normalization, and quality control were performed using miRNA QC Tool software.
2013-03-01 | E-GEOD-33568 | biostudies-arrayexpress
Project description:Expression profile of human GEP-NET tumors, including 113 fresh frozen biopsies of primary and metastatic tumours originating from pancreas (P-NET, 83 primary and 30 metastasis), 81 from small intestine (SI-NET, 44 primary and 37 metastasis), and 18 from rectum (RE-NET, 3 primary and 15 metastasis).
2018-02-25 | GSE98894 | GEO
Project description:Exposure to the olfactory receptor 51E1 agonist nonanoic acid alters small intestinal neuroendocrine tumor phenotype
| PRJNA892020 | ENA
Project description:Part I - SI-NET tumors High Resolution Isoelectric Focusing (HiRIEF) LC-MS and relative quantification by iTRAQ 8-plex was used to analyze 14 small intestinal neuroendocrine tumors (SI-NETs). The data was obtained from two separate TMT10plex sets and linked by a single internal pooled standard. The internal pooled standard was made by combining equal aliquots of the tryptic peptide mixtures from each of the 14 tissue samples. iTRAQ set1 was composed of 7 SI-NET samples, all from different individuals, and internal pooled standard labelled as follows: Channel 113 (sample Screen-1 with liver metastasis), Channel 114 (sample Screen-8 with liver metastasis), Channel 115 (sample Screen-3 with liver metastasis), Channel 116 (sample Screen-2 with liver metastasis), Channel 117 (sample Screen-5 no liver metastasis), Channel 118 (sample Screen-4 no liver metastasis), Channel 119 (sample Screen-10 no liver metastasis), Channel 121 (internal pooled standard). iTRAQ set2 was composed of 7 SI-NET samples, all from different individuals, and internal pooled standard labelled as follows: Channel 113 (sample Screen-7 with liver metastasis), Channel 114 (sample Screen-11 with liver metastasis), Channel 115 (sample Screen-13 with liver metastasis), Channel 116 (sample Screen-6 no liver metastasis), Channel 117 (sample Screen-12 no liver metastasis), Channel 118 (sample Screen-9 no liver metastasis), Channel 119 (sample Screen-14 no liver metastasis), Channel 121 (internal pooled standard). Part II - time course profiling in cell lines High Resolution Isoelectric Focusing (HiRIEF) LC-MS and relative quantification by TMT 10-plex was used to analyze cellular response to the neddylation inhibitor pevonedistat (MLN4924) at different timepoints in two SI-NET (small intestinal neuroendocrine tumors) cell lines. The data was obtained from two separate TMT 10-plex experiments. TMT set1 includes a time course experiment upon pevonedistat treatment of CNDT2 cells with harvests at 2h, 6h, 12h and 24h after treatment as well as of untreated control cells. Isobaric tag labelling of peptide samples with TMT10plex was used as follows. Biological duplicate controls (TMT channels 126, 127N), duplicate 2h (127C, 128N), duplicate 6h (128C, 129N), duplicate 12h (129C, 130N) and duplicate 24h (130C, 131) samples were employed. TMT set2 includes a time course experiment upon pevonedistat treatment of HC45 cells with harvests at 2h, 6h, 12h and 24h after treatment as well as of untreated control cells. Isobaric tag labelling of peptide samples with TMT10plex was used as follows. Biological duplicate controls (TMT channels 126, 127N), duplicate 2h (127C, 128N), duplicate 6h (128C, 129N), duplicate 12h (129C, 130N) and duplicate 24h (130C, 131) samples were employed.
2020-12-09 | PXD009877 | Pride
Project description:Olfactory ensheathing cells are one of the few central nervous system regenerative cells discovered so far. It is characterized by its lifelong nerve regeneration function, and it can also release a variety of neurotrophic factors and neural adhesion molecules. It is considered to be the glial cell with the strongest myelination ability. Olfactory ensheathing cells and Schwann cells have phenotypes in common, they can promote axon regeneration(R. Doucette, 1995). Olfactory ensheathing cells have the characteristics of Schwann cells and astrocytes, but the overall performance tends to be the former, which has two unique characteristics. First, it exists not only in the peripheral nerves (Schwann cells), but also in the central nervous system (astroglia); second, the olfactory mucosa has the ability to regenerate life-long, including human olfactory ensheathing cells(J. C. Bartolomei and C. A. Greer, 2000). Regeneration is a process in which olfactory ensheathing cells participate in efficient regulation, although the specific mechanism is not yet clear. Olfactory ensheathing cells are different from astrocytes and Schwann cells, but at the same time have the characteristics of these two cells(S. C. Barnett, 2004), like Schwann cells help axon growth, but more than Schwann cells It can make axons grow long distances, that is, it has stronger migration(A. Ramon-Cueto et al., 1998); there are also astrocytes that have a nutritional effect on the survival of neurons and the growth of axons, but olfactory ensheathing cells can also wrap neurons forms myelin sheath to support the growth of nerve processes(R. Devon and R. Doucette, 1992; J. Gu et al., 2019). There are two characteristics that make olfactory ensheathing cells the best choice for the treatment of neurological diseases(S. C. Chiu et al., 2009; J. Kim et al., 2018; M. Abdel-Rahman et al., 2018). Olfactory ensheathing cells are gradually used to treat spinal cord injuries and have shown amazing effects(J. C. Bartolomei and C. A. Greer, 2000; K. J. Liu et al., 2010; R. Yao et al., 2018). Olfactory ensheathing cells that have been used in research are usually derived from the olfactory bulb(E. H. Franssen et al., 2007), but it is easier to obtain olfactory ensheathing cells from the olfactory mucosa in clinical practice(M. Ryszard et al., 2006), so the difference between the olfactory ensheathing cells from the olfactory bulb and the olfactory mucosa There are more and more studies(B. M. U. et al., 2007), and previous studies have shown that they not only have many similar functions, but also have many differences(M. W. Richter et al., 2005; L. Wang et al., 2014; K. E. Smith et al., 2020). Because olfactory ensheathing cells derived from the olfactory bulb are not easy to obtain, olfactory ensheathing cells derived from the olfactory mucosa have become the focus of attention. Although we know that olfactory ensheathing cells from two sources have nerve repair functions, it is not clear why the two different sources of olfactory ensheathing cells have different therapeutic effects. Nicolas G. once studied that the genetic difference between the two cells and found that there are many genes related to wound repair and nerve regeneration(G. Nicolas et al., 2010). We have reason to guess that olfactory ensheathing cells from these two sources will also have a large difference in protein level. Our research group wants to use the current mature transcriptome and proteomic sequencing technologies to explore the difference between olfactory ensheathing cells from the olfactory bulb and olfactory mucosa, and explain why the two sources of olfactory ensheathing cells shows different therapeutic effects, hope to provide a new theoretical basis for future clinical treatment.
2022-02-16 | PXD024046 | Pride
Project description:Neurotoxicity of formaldehyde (FA) in the human health attracted intensive studies Long-term exposure to FA leads to learning and memory decline and is responsible for the multiple chemical sensitivity (MCS) or sick building syndrome (SBS). It was cleared that Formaldehyde impairs Learning and Memory in Hippocampal. however ,it is unclear if FA can disturb the olfactory bulb function miRNAs alterations were related to environmental chemical exposure. It was reported that FA inhale altered miRNAs expression in the nasal Epithelium and lung cells. In the present study, FA inhalation significatly alters miRNA expression profiles within olfactory bulb
2015-08-04 | GSE59369 | GEO
Project description:To investigate the relation of small intestine neuroendocrine tumor (SI-NET) properties and epigenetics to normal human enteroendocrine cell differentiation [scATAC-seq] We established Neurog3ER inducible cell lines and then performed chromatin analysis at single cell level using data obtained from normal EEC single cell ATAC-seq at various time points.
2026-04-29 | GSE238273 | GEO
Project description:Neurotoxicity of formaldehyde (FA) in the human health attracted intensive studies Long-term exposure to FA leads to learning and memory decline and is responsible for the multiple chemical sensitivity (MCS) or sick building syndrome (SBS). It was cleared that Formaldehyde impairs Learning and Memory in Hippocampal. however ,it is unclear if FA can disturb the olfactory bulb function miRNAs alterations were related to environmental chemical exposure. It was reported that FA inhale altered miRNAs expression in the nasal Epithelium and lung cells. In the present study, FA inhalation significatly alters miRNA expression profiles within olfactory bulb Eight week ICR male mouse. Mice were randomly assigned to three groups. The FA group exposed to 3ppm FA for six hours for consecutive 1 and 7days in a chamber which was described previously. The standard group was kept in same condition except the FA. After expose, both group mice were deeply anesthetized with isoflurane and decapitated. The OB was rapidly dissected
2015-08-04 | E-GEOD-59369 | biostudies-arrayexpress
Project description:Mutationally silent small intestinal neuroendocrine tumors (SI-NETs) characterized by few recurrent alterations, such as those that inactivate the cyclin-dependent kinase (CDK) inhibitor CDKN1B in <10% of cases are not well defined at the molecular level. Since the native enteroendocrine cells (EECs), which these tumors resemble, are scarce; the lack of reference data from normal EECs limits identification of gene and cis-element dysregulation in SI-NETs. We established transcriptional landscapes (RNA-seq) in bulk cultures and at single-cell (sc) resolution during the trajectory of normal human EEC differentiation from ileal stem cells in vitro (PMID 38733993). We compared the findings in SI-NETs against the novel reference profiles of normal human EEC differentiation and maturation. SI-NETs correspond principally to mature EC cells, with discernible features of non-EC and progenitor cells; persistent expression of the latter genes likely contributes to malignant properties. Underlying this aberrant expression pattern we found diverse SI-NET enhancers. EECs normally differentiate through an intermediate HES6hi/ASCL1+ oscillatory state before NEUROD1+ pre-terminal cells emerge; ASCL1 expression then persists only in mature EC cells. In contrast, although SI-NETs express NEUROD1, they strictly lack ASCL1 and other genes normally co-expressed with ASCL1. Notably, ASCL1 and loci encoding transcription factors that define non-EC cell types (ISL1, ARX, PAX6, PDX1) are marked with H3K27me3, signifying epigenetic silencing. SI-NETs express CDKN1B but other CDK inhibitors, e.g., CDKN2A and CDKN1C, are epigenetically silenced, suggesting that tumor cells may especially depend on wild-type CDKN1B function. Chromatin and transcriptional features of SI-NETs, revealed for the first time with respect to normal EEC differentiation, will help identify tumorigenic pathways and candidate therapeutic targets.
2026-04-29 | GSE277212 | GEO
Project description:Mutationally silent small intestinal neuroendocrine tumors (SI-NETs) characterized by few recurrent alterations, such as those that inactivate the cyclin-dependent kinase (CDK) inhibitor CDKN1B in <10% of cases are not well defined at the molecular level. Since the native enteroendocrine cells (EECs), which these tumors resemble, are scarce; the lack of reference data from normal EECs limits identification of gene and cis-element dysregulation in SI-NETs. We established transcriptional landscapes (RNA-seq) in bulk cultures and at single-cell (sc) resolution during the trajectory of normal human EEC differentiation from ileal stem cells in vitro (PMID 38733993). We compared the findings in SI-NETs against the novel reference profiles of normal human EEC differentiation and maturation. SI-NETs correspond principally to mature EC cells, with discernible features of non-EC and progenitor cells; persistent expression of the latter genes likely contributes to malignant properties. Underlying this aberrant expression pattern we found diverse SI-NET enhancers. EECs normally differentiate through an intermediate HES6hi/ASCL1+ oscillatory state before NEUROD1+ pre-terminal cells emerge; ASCL1 expression then persists only in mature EC cells. In contrast, although SI-NETs express NEUROD1, they strictly lack ASCL1 and other genes normally co-expressed with ASCL1. Notably, ASCL1 and loci encoding transcription factors that define non-EC cell types (ISL1, ARX, PAX6, PDX1) are marked with H3K27me3, signifying epigenetic silencing. SI-NETs express CDKN1B but other CDK inhibitors, e.g., CDKN2A and CDKN1C, are epigenetically silenced, suggesting that tumor cells may especially depend on wild-type CDKN1B function. Chromatin and transcriptional features of SI-NETs, revealed for the first time with respect to normal EEC differentiation, will help identify tumorigenic pathways and candidate therapeutic targets.
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