Effect of exosomal miRNA of cancer-associated adipocyte (CAA) on the malignant transformation of pancreatic ductal adenocarcinoma
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PROVIDER: PRJNA961763 | ENA |
REPOSITORIES: ENA
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Project description:CAAs were generated by co-culturing human adipocytes with a human pancreatic cancer cell line (Panc-1), and exosomes were isolated from the CAA-conditioned medium (CAA-CM). We then performed gene expression profiling analysis using small RNA-seq of three differernt CAA-CMs and normal A-CMs.
2025-04-01 | GSE230561 | GEO
Project description:Sympathetic activation during cold exposure increases adipocyte thermogenesis via the expression of mitochondrial protein uncoupling protein 1 (UCP1)1. The propensity of adipocytes to express UCP1 is under a critical influence of the adipose microenvironment and varies between sexes and among various fat depots2-7. Here, we report that cold-induced adipocyte UCP1 expression in a female mouse subcutaneous white adipose tissue (scWAT) is regulated by mammary gland ductal epithelial cells in the adipose niche. Single-cell RNA-sequencing (scRNA-seq) shows that glandular luminal epithelium subtypes express transcripts that encode secretory factors in controlling adipocyte UCP1 expression under cold conditions. We term luminal epithelium secretory factors as “mammokines”. Using whole-tissue immunofluorescence 3D visualization, we reveal previously undescribed sympathetic nerve-ductal points of contact. We show sympathetic nerve-activated mammary ducts limit adipocyte UCP1 expression via lipocalin 2. Both in vivo and ex vivo ablation of mammary ductal epithelium enhances cold-induced scWAT adipocyte thermogenic gene program. Since the mammary duct network extends throughout most scWATs in female mice, females show markedly less scWAT UCP1 expression, fat oxidation, energy expenditure, and subcutaneous fat mass loss compared to male mice, implicating sex-specific roles of mammokines in adipose thermogenesis. These results show a previously uncharacterized role of sympathetic nerve-activated glandular epithelium in adipocyte UCP1 expression and suggest an evolutionary function of mammary duct luminal cells in defending glandular adiposity during cold exposure. Overall, our findings highlight mammary gland epithelium as a highly active metabolic cell type and implicate a broader role of mammokines in controlling female adipose metabolism, mammary gland physiology, and systemic energy homeostasis.
2023-05-01 | GSE231394 | GEO
Project description:Adipocyte-Derived Exosomal microRNAs in subject serum samples
| PRJNA516594 | ENA
Project description:Mammary ductal epithelium controls cold-induced adipocyte thermogenic program
| PRJNA965904 | ENA
Project description:The nephrotoxic ifosfamide-metabolite chloroacetaldehyde (CAA) induces changes in intracellular Ca2+-concentration of human RPTEC. This effect is due to a PKA-dependent inhibition of Na+/Ca2+ exchange (Benesic, A., Schwerdt, G. at. al. (2005) Kidney Int 68, 2029-2041). Thus, possible effects of CAA-exposure on cAMP and Ca2+ regulated genes as well the Ca2+/NFAT pathway were investigated by cDNA-microarray analysis. Both microarrays (cAMP/Ca2+ and Ca2+(NFAT) were performed twice. After 24 h CAA exposure a marked downregulation of c-fos and junB was observed in all arrays performed. In the cAMP/Ca2+-arrays downregulation of FOS, ADRB1, INHBA, CDK5, IL2, PLN, SRF, GCG, SGK, JUNB, BDNF, S100A6, CCNA1, MIF, HK2, SST and EGR2 by CAA was observed in two independent experiments. From the AP-1 family expression of junD and fosB were not altered. Overexpression by CAA of CREB and DDIT3 were only observed in one of two experiments. JUND, FOSB, FOSL1, CREM and CREBBP expression was not influenced in reproducible manner, as well as all members of the NFAT-family. In the Ca2+/NFAT-Arrays, PPP3CB, VAV3, NFATC1, IL8, IL6, FASLG, IL3, IFNB1, FOS, BCL2, EGR3, CD3G, HRAS, EP300, IL4, CALM3, RELA, EGR2, NPPB, IFNG, NFATC4, KPNA5, CAMK2BNFKB2 , VEGF, IL8RA, IL2,GATA4, MEF2A, PTPRC, ICOS, NFKBIE, CDKN1A, CSNK2B, ACTB, MEF2B and JUNB mRNA´s were repeatedly reduced by CAA exposure. The only gene with upregulation in both experiments was found to be IFN-alpha. Thus CAA exposure for 24 h leads to a downregulation of of the AP-1 members JUNB and FOS, whereas there is small positive effect on CREB mRNA. CAA reproducibly lowers the expression of IL-2, 3, 4, 6 and 8, whereas the levels of TNFalpha and TGFbeta1 and 3 mRNA were not altered. IFN-alpha mRNA levels were reproducibly increased (>2-fold). In conclusion, CAA seems to interact with Ca2+ and cAMP signalling pathways, with a strong impact on AP-1 proteins and inflammatory signalling. Keywords: stress response to toxic agent
2006-06-30 | GSE4956 | GEO
Project description:Background:Exosomes are extracellular vesicles secreted by a variety of cells and are widely distributed in human body fluids. Exosomal long non-coding RNA (lncRNA) is a by-product of gene transcription and is involved in the regulation of cancer cell growth and migration. Numerous studies have identified aberrant lncRNA levels in pancreatic cancer (PC), but studies on exosomal lncRNA expression in pancreatic ductal adenocarcinoma (PDAC) plasma are relatively few and remain largely unknown. Methods:We studied the expression of exosomal lncRNAs and mRNAs in the plasma of 5 PDAC patients and 5 healthy human subjects using high-throughput sequencing. Results:A total of 43715 exosomal lncRNAs were found to be expressed in PDAC and healthy human plasma, of which 5851 were up-regulated, and 1055 were down-regulated in all 5 PDAC plasma (≥2.0-fold change, P<0.05). The expression of eight significantly expressed genes (ABCD4, RP11-77P6.2, FLVCR1-AS1, HMBOX1, TUBA1C, RP11-115C21.2, PRKG1-AS1, and MTATP6P1) were selected to be measured in 5 patients using database and real-time quantitative reverse transcription PCR (qRT-PCR), and the data were consistent with those obtained from high-throughput sequencing. Analysis of their nearby coding genes (mRNAs) showed that the principal functions of most genes were to regulate cell metabolism process, apoptosis, protein binding and receptor binding. The main regulatory pathways included the ErbB signaling pathway, which regulates cell proliferation and differentiation, and the tumour pathway. Analysis of the co-expressed gene regulatory network identified key lncRNA-mRNA pairs that may play an important role in the pathogenesis of PDAC. Conclusions: Expression differences in exosomal lncRNAs exist between PDAC and healthy human plasma, so the expression profile of exosomal lncRNAs could explain the onset and development of PDAC and could also serve as a candidate biomarker for the diagnosis of PDAC and a potential therapeutic target.
2022-01-01 | GSE175436 | GEO
Project description:We profiled miRNAs in 3T3-L1 adipocyte-secreted exosomes and our microarray analysis revealed that more than 300 exosomal miRNAs were detected during adipocyte differentiation.
2021-01-24 | GSE154875 | GEO
Project description:Expression profile of exosomal LncRNA in plasma of pancreatic ductal adenocarcinoma
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Project description:Affymetrix miRNA 4.0 array profiling of adipocyte-derived exosomes from lean and obese subjects. We used miRNA arrays to profile FABP4+ (adipocyte-derived) exosomes isolated from serum of lean and obese subjects.
2019-06-03 | GSE125494 | GEO
Project description:Gonolobinae: Caa
| PRJEB37028 | ENA