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SFPQ promotes an oncogenic transcriptomic state in melanoma

ABSTRACT: SFPQ promotes an oncogenic transcriptomic state in melanoma

PROVIDER: PRJNA719095 | ENA |

REPOSITORIES: ENA

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SFPQ promotes an oncogenic transcriptomic state in melanoma

Project description:Analysis of SFPQ interactome in primary melanocytes and melanoma cells. Results provide insight into the oncogenic reprogamming of SFPQ-RNA interactome and especially the interactions with key melanoma-associated coding transcripts.

2021-06-30 | GSE171291 | GEO

SFPQ promotes an oncogenic transcriptomic state in melanoma.

Project description: Not available

| S-EPMC8376646 | biostudies-literature

Microarray of zebrafish (Danio rerio) sfpq-/-;Tg(mnx1:GFP) against sfpq+/+;Tg(mnx1:GFP) and sfpq+/-;Tg(mnx1:GFP) siblings at 24 hpf

Project description:Phenotypic characterisation of our zebrafish sfpq homozygous mutants revealed a restricted set of specific defects, unexpected for a protein expressed ubiquitously and involved in such general mechanisms. The CNS was prominently affected, showing brain boundary and axonal defects associated with absence of motility. To investigate a possible specificity in SFPQ functional targets by microarray RNA profiling analysis, comparing the transcriptome of the sfpq homozygous mutants with its wild type and heterozygous siblings at the earliest stage at which the phenotype is robustly recognizable.

2017-09-01 | E-MTAB-5559 | biostudies-arrayexpress

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma

Project description:Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma

| PRJNA636815 | ENA

Anatomic position determines oncogenic specificity in melanoma

Project description:Oncogenic alterations to DNA are not transforming in all cellular contexts. This may be due to pre-existing transcriptional programs in the cell of origin. Here, we define anatomic position as a major determinant of why cells respond to specific oncogenes. Cutaneous melanoma arises throughout the body, whereas the acral subtype arises on the palms of the hands, soles of the feet, or under the nails. We sequenced the DNA of cutaneous and acral melanomas from a large cohort of human patients and found a specific enrichment for BRAF mutations in cutaneous melanoma but CRKL amplifications in acral melanoma. We modeled these changes in transgenic zebrafish models and found that CRKL-driven tumors predominantly formed in the fins of the fish. The fins are the evolutionary precursors to tetrapod limbs, indicating that melanocytes in these acral locations may be uniquely susceptible to CRKL. RNA profiling of these fin/limb melanocytes, compared to body melanocytes, revealed a positional identity gene program typified by posterior HOX13 genes. This positional gene program synergized with CRKL to drive tumors at acral sites. Abrogation of this CRKL-driven program eliminated the anatomic specificity of acral melanoma. These data suggest that the anatomic position of the cell of origin endows it with a unique transcriptional state that makes it susceptible to only certain oncogenic insults.

2022-01-12 | PXD027968 | Pride

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [tfap2a/e]

Project description:Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [tfap2a/e]

| PRJNA636816 | ENA

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [2D culture]

Project description:Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [2D culture]

| PRJNA636817 | ENA

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [3D culture]

Project description:Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [3D culture]

| PRJNA636818 | ENA

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [RNA-Seq]

Project description:Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [RNA-Seq]

| PRJNA641144 | ENA

SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells II

Project description:Oncoproteins such as the BRAFV600E kinase entrust cancer cells with malignant properties, but they also create unique vulnerabilies. Therapeutic targeting of the BRAFV600E-driven cytoplasmic signaling network has proven ineffective, since patients regularly relapse with reactivation of the targeted signaling pathways. Here, we identified the nuclear protein SFPQ to be synthetically lethal with BRAFV600E in a loss-of-function shRNA screen. SFPQ depletion decreased proliferation and induced apoptosis in BRAFV600E-driven colorectal and melanoma cells, and reduced tumor growth in xenografts. Mechanistically, SFPQ loss in BRAF-mutant cancer cells triggered the Chk1-dependent replication checkpoint, resulting in replication stress in the absence of overt DNA damage. Affected cells stalled in S-Phase with hallmark signs of impaired replication factories. Induction of BRAFV600E and concomitant loss of SFPQ sensitized cells to a combination of DNA replication checkpoint inhibitors and chemically induced replication stress, pointing towards future therapeutic approaches exploiting nuclear vulnerabilities induced by BRAFV600E.

2020-04-27 | GSE149370 | GEO

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