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Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

ABSTRACT: Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

PROVIDER: PRJNA1143060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR30104730_1.fastq.gz	Fastqsanger.gz
	SRR30104730_2.fastq.gz	Fastqsanger.gz
	SRR30104731_1.fastq.gz	Fastqsanger.gz
	SRR30104731_2.fastq.gz	Fastqsanger.gz

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Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

Project description:Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

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Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

Project description:Bulk RNAseq was performed to identify differences in gene expression in SKMEL28 cells as related to MITF and TFE3 expression.

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Melanoma plasticity is regulated by mTOR-mediated crosstalk between MITF and TFE3

Project description:ATAC-seq performed to identify chromatin accessibility across the genome. CUT&RUN-seq was performed to identify and compare transcription factor and histone mark occupancy across genome of WT and MITF and TFE3 KO cells.

2025-03-20 | GSE273815 | GEO

Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

Project description:To understand the activation of the MITF/TFE transcription factors in effective defense against pathogens we examined the genome wide distribution of TFE3 in control and activated mouse macrophages. It was determined that TFEB and TFE3 collaborate with each other to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of proinflammatory cytokines and key mediators of the inflammatory response. 4 samples were analyzed: Background Control, Control, Starvation, LPS

2016-02-01 | E-GEOD-75822 | biostudies-arrayexpress

Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

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Antagonistic Roles for MITF and TFE3 in Melanoma Plasticity.

Project description:Melanoma cells have the ability to switch from a melanocytic and proliferative state to a mesenchymal and invasive state and back again. This plasticity drives intra-tumoral heterogeneity, progression, and therapeutic resistance. Microphthalmia-associated Transcription Factor (MITF) promotes the melanocytic/proliferative phenotype, but factors that drive the mesenchymal/invasive phenotype and the mechanisms that effect the switch between cell states are unclear. Here, we identify the MITF paralog TFE3 and the non-canonical mTORC1 pathway as regulators of the mesenchymal state. We show that TFE3 expression drives the metastatic phenotype in melanoma cell lines and tumors. Deletion of TFE3 in MITF-low melanoma cell lines suppresses their ability to migrate and metastasize. Further, MITF suppresses the mesenchymal phenotype by directly or indirectly activating expression of FNIP1, FNIP2, and FLCN, which encode components of the non-canonical mTORC1 pathway, thereby promoting cytoplasmic retention and lysosome-mediated degradation of TFE3. These findings highlight a molecular pathway controlling melanoma plasticity and invasiveness.

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The crosstalk between MYC and mTOR during osteoclastogenesis

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DETECTION OF FOUR NOVEL RENAL TUMORS CASES HARBORING RBM10-TFE3 FUSIONS

Project description:Microphtalmia-associated-transcriptional-factor-family translocation renal cell carcinoma (MiTF-tRCC) currently includes two main subtypes: “TFEB-tRCC” most often characterized by a t(6;11)(p21;q13) that generates a fusion of TFEB with MALAT1 and “TFE3-tRCC” characterized by rearrangements of TFE3 at Xp11.23 (2-3) that produce a variety of fusion genes. FISH is a handy method in routine practice that allows the detection of a rearrangement of TFE3. However, it reaches its limits in cases of micro-inversions or insertions: in fact paracentric microinversions that involve GRIPAP1 (Xp11.23) (23, Classe) or RBM10 (Xp11.3), very close to TFE3 , are most often undetectable.We report the clinical, immunohistological, genomic and molecular description of four novel TFE3-tRCC with RBM10-TFE3 fusion detected by targeted RNASeq analysis that illustrate the difficulties of diagnosis, especially in reason of disconcerting negative TFE3 FISH results.

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Project description:The ability of cancer cells to switch phenotype in response to a dynamic intra-tumor microenvironment is a major barrier to effective therapy. In melanoma, down-regulation of the lineage addiction oncogene MITF (Microphthalmia-associated transcription factor) is a hallmark of the proliferative-to-invasive phenotype switch. Yet how MITF promotes proliferation and suppresses invasion is poorly understood. Here we show that expression of the key lipogenic enzyme stearoyl-CoA desaturase (SCD) is activated by MITF, but suppressed by the stress-responsive transcription factor ATF4. SCD expression is required for MITF-positive melanoma cell proliferation,. By contrast, MITF-low cells express reduced levels of SCD and are insensitive to its inhibition, indicating that cell phenotype dictates response to drugs targeting lipid metabolism. Since SCD suppresses inflammatory signalling and ATF4 expression, the results identify a positive feedback-loop that can maintain an invasive phenotype, uncover a key role for MITF and ATF4 in metabolic reprograming, and reveal fatty acid composition as a driver of melanoma phenotype-switching.

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Mapping of the master transcription factor MITF in prostate cancer

Project description:“Mi” transcription family members such as TFE3 and TFEB, participate in the pathogenesis of a subgroup of renal cell carcinomas, whereas MITF is key in melanocyte development and also contributes to melanoma, behaving as an oncogene when amplified and facilitating tumor invasiveness and therapy resistance when MITF levels are low. In addition, MITF plays a role in the survival and growth of clear cell sarcoma and pancreatic cancer. In prostate cancer MITF through the regulation of the heat-shock protein CRYAB has been suggested to suppress tumor initiation. However, the role of MITF in advanced therapy resistant lethal stages of the disease remains unknown. To gain insight into the gene network regulated by MITF in prostate cancer, we mapped MITF genomewide in a human prostate cancer cell line (22Rv1) by chromatin immunoprecipitation followed by ultra high-throughput sequencing. This analysis revealed the genomewide locations of MITF in prostate cancer, including the promoter of eIF3B which we further functionally validated through ChIP-PCR and luciferase reporter assays. We propose that the master regulator MITF by regulating a distinct gene network may play key roles in suppressing lethal prostate cancer pathogenesis.

2023-12-22 | GSE237870 | GEO

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