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Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

ABSTRACT: Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

PROVIDER: PRJNA528278 | ENA |

REPOSITORIES: ENA

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Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

Project description:Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitochondria are inhibited in cybrids with non-cancerous mitochondria. These results suggest the critical oncogenic regulation by motochondrial-nuclear cross talk and highlights rectifying motochondiral functional properties as a promising target in cancer therapy.

2019-03-21 | GSE128610 | GEO

Crosstalk from non-cancerous mitochondria can inhibit tumor properties of metastatic cells by suppressing oncogenic pathways.

Project description: Not available

| S-EPMC3650012 | biostudies-literature

Correction: Crosstalk from Non-Cancerous Mitochondria Can Inhibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways.

Project description: Not available

| S-EPMC6706049 | biostudies-literature

Crosstalk between gut microbiota and mitochondria during endurance: a new example of holobiont in mammals

Project description:Endurance exercise has a dramatic impact on the functionality of mitochondria and on the composition of intestinal microbiome, but the mechanisms regulating the crosstalk between these two components are still largely unknown. Here, we sampled 20 elite horses before and after an endurance race and used blood transcriptome, blood metabolome and fecal microbiome to describe the microbiota-mitochondria inter-talk. A subset of mitochondria-related differentially expressed genes involved in pathways such as energy metabolism, oxidative stress and inflammation was discovered and then shown to be associated with butyrate-producing bacteria of the Lachnospiraceae family, especially Eubacterium. The mechanisms involved were not fully understood, but through the action of their metabolites likely acted on PPARδ, the FRX-CREB axis and their downstream targets to delay the onset of hypoglycemia, inflammation and extend running time. Our results also suggested that circulating free fatty acids may act not merely as fuel but drive mitochondrial inflammatory responses triggered by the translocation of gut bacterial polysaccharides following endurance. Targeting the gut-mitochondria axis appears therefore as a potential strategy to enhance athletic performance.

2021-02-09 | GSE163767 | GEO

miR-24 induces human T cell exhaustion though mitochondria energy metabolic reprograming via suppressing MYC and FGF11

Project description:Exhausted T cells (TExh) is a barrier for cancer immunotherapy, evidences demonstrate that transcriptional regulation is essential for TEX induction; however the factors that manipulate exhausted phenotype are largely unexplored. Here we showed that the microRNA (miR)-24, previously established to be enriched in eoxosmes from nasopharyngeal carcinoma (NPC) cells and promote T cell dysfunction, induced T cells to express high level of TIM-3, PD-1 and CD39 but to display low IFNg and GrB secretion and diminished proliferation ability ( a TExh phenotype) through inhibiting energy metabolism in vitro. Forced miR-24 expression inhibited ATP production through mitochondrial oxidative phosphorylation, while blockade of endogenous miR-24 the mitochondrial formation became massive and tubular and the levels of mitochondrial constituent proteins including Mfn1, Mfn2, P-Drp1 and TOMM20 was increased in OKT-3 stimulated T cells. MiR-24-mediated TEX and mitochondria metabolism reprogramming were regulated by suppressing MYC and FGF11 expression. Moreover, MYC enhanced the FGF11 transcription to promote mitochondria ATP production. Importantly, clinical data showed an increased TEX phenotype in circuiting and tumor-infiltrating T cells from NPC patients. Thus, our findings support that inhibition of miR-24-mediated mitochondria metabolism reprogramming can be titrated to break TExh immune barrier in NPC immunotherapy.

2020-08-11 | GSE110523 | GEO

Gene expression profile of cancerous and non-cancerous renal tissues

Project description:Gene expression profile of cancerous and non-cancerous renal tissues

| PRJNA714233 | ENA

DNA methylation profile of cancerous and non-cancerous renal tissues

Project description:DNA methylation profile of cancerous and non-cancerous renal tissues

| PRJNA701825 | ENA

Crosstalk between gut microbiota and mitochondria during endurance: a new example of holobiont in mammals

Project description:Crosstalk between gut microbiota and mitochondria during endurance: a new example of holobiont in mammals

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Normal and Cancerous Prostate Cells

Project description:This SuperSeries is composed of the following subset Series: GSE38674: Genomic DNA in Normal and Cancerous Prostate Cells GSE38676: Expression Analysis of Normal and Cancerous Prostate Cells GSE38677: Mapping of Transcription Start Sites of Normal and Cancerous Prostate Cells GSE38682: H3K4me3 Marks in Normal and Cancerous Prostate Cells GSE38683: H3K27me3 Marks in Normal and Cancerous Prostate Cells GSE38684: Chromatin Looping of Normal and Cancerous Prostate Cells Refer to individual Series

2012-10-16 | E-GEOD-38685 | biostudies-arrayexpress

Paired non-cancerous and cancerous miRNA expression of esophageal adenocarcinoma and squamous cell carcinoma patients

Project description:Identifying biomarkers predictive for early esophageal cancer detection is critical considering the dismal survival rates. We investigated the involvement of microRNAs (miRNAs), their utility as biomarkers, and their association with survival in esophageal cancer, including Barrett’s associated and sporadic adenocarcinoma (ADC), and squamous cell carcinoma (SCC). MiRNA expression was measured in cancerous and adjacent non-cancerous tissue pairs collected from 76 US and Japanese patients enrolled in 3 distinct cohorts. In ADC patients, miR-21, miR-194, miR-293, and miR-223 expression was elevated, while miR-375 and miR-203 expression was reduced in cancerous tissue compared to non-cancerous tissue. Increased levels of miR-192 and miR-194 were observed in Barrett’s associated compared to sporadic ADC cancerous tissue. In SCC patients, miR-21, miR-181b, miR-155, and miR-146b expression was elevated while miR-375 and miR-203 levels were reduced in cancerous tissue compared to non-cancerous tissue. Significantly, elevated mir-21 expression in non-cancerous tissue was strongly associated with worse prognosis, independent of nodal status and age. Sample classification using miRNA expression yielded accuracies as high as 86% for diagnosis and 78% for Barrett’s esophagus status. Our results highlight that miRNAs are deregulated in esophageal carcinogenesis and Barrett’s esophagus, and that their expression is associated with survival in cancer patients. Sample classification using miRNA expression demonstrates their potential utility as biomarkers for esophageal carcinoma diagnosis.

2010-07-09 | GSE13937 | GEO

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