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Thymidylate synthase maintains the de-differentiated state of triple negative breast cancers

ABSTRACT: Thymidylate synthase maintains the de-differentiated state of triple negative breast cancers

PROVIDER: PRJNA506989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8244640.fastq.gz	Fastqsanger.gz
	SRR8244641.fastq.gz	Fastqsanger.gz
	SRR8244642.fastq.gz	Fastqsanger.gz
	SRR8244643.fastq.gz	Fastqsanger.gz

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Thymidylate synthase maintains the de-differentiated state of triple negative breast cancers

Project description:Cancer cells frequently boost nucleotide metabolism (NM) to support their increased proliferation, but the consequences of elevated NM on tumor de-differentiation are mostly unexplored. Here, we identified a role for thymidylate synthase (TS), a NM enzyme and established drug target, in cancer cell de-differentiation and investigated its clinical significance in breast cancer (BC). In vitro, TS knockdown increased the population of CD24+ differentiated cells, and attenuated migration and sphere-formation. RNA-seq profiling indicated a repression of epithelial-to-mesenchymal transition (EMT) signature genes upon TS knockdown, and TS-deficient cells showed an increased ability to invade and metastasize in vivo, consistent with the occurrence of a partial EMT phenotype. Mechanistically, TS enzymatic activity was found essential for the maintenance of the EMT/stem-like state by fueling a dihydropyrimidine dehydrogenase – dependent pyrimidine catabolism. In patient tissues, TS levels were found significantly higher in poorly differentiated and in triple negative BC, and strongly correlated with worse prognosis. The present study provides the rationale to study in-depth the role of NM at the crossroads of proliferation and differentiation, and depicts new avenues for the design of novel drug combinations for the treatment of BC

2019-02-01 | GSE122953 | GEO

Thymidylate synthase maintains the de-differentiated state of triple negative breast cancers.

Project description:Cancer cells frequently boost nucleotide metabolism (NM) to support their increased proliferation, but the consequences of elevated NM on tumor de-differentiation are mostly unexplored. Here, we identified a role for thymidylate synthase (TS), a NM enzyme and established drug target, in cancer cell de-differentiation and investigated its clinical significance in breast cancer (BC). In vitro, TS knockdown increased the population of CD24+ differentiated cells, and attenuated migration and sphere-formation. RNA-seq profiling indicated repression of epithelial-to-mesenchymal transition (EMT) signature genes upon TS knockdown, and TS-deficient cells showed an increased ability to invade and metastasize in vivo, consistent with the occurrence of a partial EMT phenotype. Mechanistically, TS enzymatic activity was found essential for maintenance of the EMT/stem-like state by fueling a dihydropyrimidine dehydrogenase-dependent pyrimidine catabolism. In patient tissues, TS levels were found significantly higher in poorly differentiated and in triple negative BC, and strongly correlated with worse prognosis. The present study provides the rationale to study in-depth the role of NM at the crossroads of proliferation and differentiation, and depicts new avenues for the design of novel drug combinations for the treatment of BC.

| S-EPMC6888897 | biostudies-literature

Gene expression in cells expressing doxycycline-induced thymidylate synthase transgene

Project description:Gene expression was compared between a Tet-OFF transfomant expressing thymidylate synthase trasgene and its parental human colorectal cancer cell line, DLD-1, or the transformant exposed to doxycycline.

2015-03-31 | E-MTAB-3414 | biostudies-arrayexpress

Specific PBAF complex (dcPBAF) containing PHF10 lacking DPF maintains transcription in differentiated neurons

Project description:The PBAF chromatin-remodeling complex is essential for transcription in mammalian cells. We found that PHF10 specific subunit of PBAF lacking C-terminal DPF is expressed in neurons of adult mouse and human brain. We purified the neuronal PBAF of newborn and adult mouse brain using antibodies against PHF10. We found that specific PBAF, designated as dcPBAF, is dominant in mature neurons. dcPBAF is associated with TAF4, TAF5, TAF6, TAF9 subunits of TFIID, does not contain BRD7 and is characterized by the presence of PHF10 isoform lacking N-terminal amino acids and DPF. The dcPBAF binds promoters of actively transcribed housekeeping and neuron specific genes in terminally differentiated neurons of adult mouse. It maintains high transcription level of neuron specific genes in differentiated human neuronal cell. These data indicate some specific features of PBAF mediated chromatin in terminally differentiated mammalian cells.

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Specific PBAF complex (dcPBAF) containing PHF10 lacking DPF maintains transcription in differentiated neurons

Project description:Specific PBAF complex (dcPBAF) containing PHF10 lacking DPF maintains transcription in differentiated neurons

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Genomic profiling of matched well differentiated and de-differentiated liposarcoma.

Project description:Well-differentiated (WD) and de-differentiated (DD) liposarcoma, subtypes of adipocytic sarcomas, are pathologically and clinically dissimilar, but are poorly distinguishable at the molecular level. These tumors harbor neochromosomes formed from amplifications and rearrangements of chr12q. Nineteen selected patients with matched WD and DD tumors underwent extensive exomic and transcriptomic profiling to distinguish genomic features between the two subtypes. Shared point mutations suggest a common tumor origin and de-differentiated tumors have higher burdens of deletions.

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Small RNA profiling of differentiated and de-differentiated vascular smooth muscle cell

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Thymidylate synthase drives the phenotypes of epithelial-to-mesenchymal transition in non-small cell lung cancer

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De novo lipogenesis maintains vascular homeostasis through endothelial nitric-oxide synthase (eNOS) palmitoylation.

Project description:Endothelial dysfunction leads to lethal vascular complications in diabetes and related metabolic disorders. Here, we demonstrate that de novo lipogenesis, an insulin-dependent process driven by the multifunctional enzyme fatty-acid synthase (FAS), maintains endothelial function by targeting endothelial nitric-oxide synthase (eNOS) to the plasma membrane. In mice with endothelial inactivation of FAS (FASTie mice), eNOS membrane content and activity were decreased. eNOS and FAS were physically associated; eNOS palmitoylation was decreased in FAS-deficient cells, and incorporation of labeled carbon into eNOS-associated palmitate was FAS-dependent. FASTie mice manifested a proinflammatory state reflected as increases in vascular permeability, endothelial inflammatory markers, leukocyte migration, and susceptibility to LPS-induced death that was reversed with an NO donor. FAS-deficient endothelial cells showed deficient migratory capacity, and angiogenesis was decreased in FASTie mice subjected to hindlimb ischemia. Insulin induced FAS in endothelial cells freshly isolated from humans, and eNOS palmitoylation was decreased in mice with insulin-deficient or insulin-resistant diabetes. Thus, disrupting eNOS bioavailability through impaired lipogenesis identifies a novel mechanism coordinating nutritional status and tissue repair that may contribute to diabetic vascular disease.

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Small RNA profiling of differentiated and de-differentiated vascular smooth muscle cell

Project description:We report the application of small RNA sequencing for high-throughput profiling of small RNA under 75 bp in vascular smooth muscle cell. By a reading depth of 30M and single stranded sequencing, we generated the small RNA signature on differentiated and de-differentiated vascular smooth muscle cell induced by PDGF-BB and H3K4me2 editing. We found that PDGF-BB and H3K4me2 editing induced de-differentiation modulated miRNA profile significantly, which was demonstrated at least in part responsible for modulated vascular smooth muscle cell phenotype.

2022-04-01 | GSE186972 | GEO

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