Critical opposing roles for TFEB andTFE3 in melanoma progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1161572 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Unlike MITF-M, the melanocyte-specific isoform of MITF, TFEB, TFE3 and non-melanocyte MITF isoforms are regulated primarily by mTORC1-mediated phosphorylation at the lysosome that promotes their cytoplasmic retention. As low levels of glucose or amino acids trigger down-regulation of MITF, it is likely that on nutrient limitation some MITF functions are assumed by TFE3 and TFEB, enabling MITFLow melanoma cells to survive and proliferate. The role TFEB and TFE3 in melanoma biology and their impact on MITF-driven proliferation is poorly understood.
2025-09-03 | GSE277250 | GEO
Project description:Unlike MITF-M, the melanocyte-specific isoform of MITF, TFEB, TFE3 and non-melanocyte MITF isoforms are regulated primarily by mTORC1-mediated phosphorylation at the lysosome that promotes their cytoplasmic retention. As low levels of glucose or amino acids trigger down-regulation of MITF, it is likely that on nutrient limitation some MITF functions are assumed by TFE3 and TFEB, enabling MITFLow melanoma cells to survive and proliferate. The role TFEB and TFE3 in melanoma biology and their impact on MITF-driven proliferation is poorly understood.
2025-09-03 | GSE270585 | GEO
Project description:Unlike MITF-M, the melanocyte-specific isoform of MITF, TFEB, TFE3 and non-melanocyte MITF isoforms are regulated primarily by mTORC1-mediated phosphorylation at the lysosome that promotes their cytoplasmic retention. As low levels of glucose or amino acids trigger down-regulation of MITF, it is likely that on nutrient limitation some MITF functions are assumed by TFE3 and TFEB, enabling MITFLow melanoma cells to survive and proliferate. The role TFEB and TFE3 in melanoma biology and their impact on MITF-driven proliferation is poorly understood.
2025-09-03 | GSE270594 | GEO
Project description:Genome-wide profiling of TFEB targets in melanoma
| PRJNA1127526 | ENA
Project description:Opposing Roles of Hepatic Stellate Cell Subpopulations in Hepatocarcinogenesis
| PRJNA873690 | ENA
Project description:Opposing roles of dendritic cells subsets in experimental GN
| PRJNA413937 | ENA
Project description:Transcription factor EB (TFEB) mainly regulates the autophagy-lysosomal pathway, associated with many diseases, including cancer. However, the role of TFEB in pan-cancer has not been investigated systematically. In this study, we comprehensively analyzed TFEB targets under three stresses in Hela cells by cross-validation of RNA-seq and ChIP-seq. 1,712 novel TFEB targets have not been reported in the Gene Set Enrichment Analysis and ChIP Enrichment Analysis databases. We further investigated their distributions and roles among the pan-cancer co-expression networks across 32 cancers constructed by multiscale embedded gene co-expression network analysis (MEGENA) based on the Cancer Genome Atlas (TCGA) cohort. Specifically, TFEB might serve as a hidden player with multifaceted functions in regulating pan-cancer risk factors, e.g., CXCL2, PKMYT1, and BUB1, associated with cell cycle and immunosuppression. TFEB might also regulate protective factors, e.g., CD79A, related to immune promotion in the tumour microenvironment. We further developed a Shiny app website to present the comprehensive regulatory targets of TFEB under various stimuli, intending to support further research on TFEB functions. Summarily, we provided references for the TFEB downstream targets responding to three stresses and the dual roles of TFEB and its targets in pan-cancer, which are promising anticancer targets that warrant further exploration.
2024-11-10 | GSE273702 | GEO
Project description:Transcription factor EB (TFEB) mainly regulates the autophagy-lysosomal pathway, associated with many diseases, including cancer. However, the role of TFEB in pan-cancer has not been investigated systematically. In this study, we comprehensively analyzed TFEB targets under three stresses in Hela cells by cross-validation of RNA-seq and ChIP-seq. 1,712 novel TFEB targets have not been reported in the Gene Set Enrichment Analysis and ChIP Enrichment Analysis databases. We further investigated their distributions and roles among the pan-cancer co-expression networks across 32 cancers constructed by multiscale embedded gene co-expression network analysis (MEGENA) based on the Cancer Genome Atlas (TCGA) cohort. Specifically, TFEB might serve as a hidden player with multifaceted functions in regulating pan-cancer risk factors, e.g., CXCL2, PKMYT1, and BUB1, associated with cell cycle and immunosuppression. TFEB might also regulate protective factors, e.g., CD79A, related to immune promotion in the tumour microenvironment. We further developed a Shiny app website to present the comprehensive regulatory targets of TFEB under various stimuli, intending to support further research on TFEB functions. Summarily, we provided references for the TFEB downstream targets responding to three stresses and the dual roles of TFEB and its targets in pan-cancer, which are promising anticancer targets that warrant further exploration.
2024-11-10 | GSE273703 | GEO
Project description:Faithful execution of developmental programs relies on the acquisition of unique cell identities from pluripotent progenitors, a process governed by combinatorial inputs from numerous signaling cascades that ultimately dictate lineage-specific transcriptional outputs. Despite growing evidence that metabolism is integrated with many molecular networks, how pathways that control energy homeostasis may affect cell fate decisions is largely unknown. Here, we show that AMPK, a central metabolic regulator, plays critical roles in lineage specification. Although AMPK-deficient embryonic stem cells (ESCs) were normal in the pluripotent state, these cells displayed profound defects upon differentiation, failing to generate chimeric embryos and preferentially adopting an ectodermal fate at the expense of the endoderm during embryoid body (EB) formation. AMPK-/- EBs exhibited reduced levels of Tfeb, a master transcriptional regulator of lysosomes, leading to diminished endolysosomal function. Remarkably, genetic loss of Tfeb also yielded endodermal defects, while AMPK-null ESCs over-expressing this transcription factor normalized their differential potential, revealing an intimate connection between Tfeb/lysosomes and germ layer specification. The compromised endolysosomal system resulting from AMPK or Tfeb inactivation blunted Wnt signaling, while up-regulating this pathway restored expression of endodermal markers. Collectively, these results uncover the AMPK pathway as a novel regulator of cell fate determination during differentiation. 2 WT and 2 AMPK DKO ESC lines were differentiated into embryoid bodies (EBs) for various lengths of time (2, 4, 8, and 12 days) in high and low glucose conditions. Both ESC and EB samples were profiled by mRNA-seq to examine how global gene expression changes associated with ESC differentiation are affected by AMPK deletion.
2016-03-09 | E-GEOD-77705 | biostudies-arrayexpress
Project description:TFEB and TFE3 are key regulators of melanoma biology
| PRJNA1127539 | ENA