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

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

PROVIDER: PRJNA625089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11540922_1.fastq.gz	Fastqsanger.gz
	SRR11540922_2.fastq.gz	Fastqsanger.gz
	SRR11540923_1.fastq.gz	Fastqsanger.gz
	SRR11540923_2.fastq.gz	Fastqsanger.gz
	SRR11540924_1.fastq.gz	Fastqsanger.gz

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

Project description:Epithelial to mesenchymal transition (EMT) is a developmental process driving metastasis and chemoresistance. Thymidylate synthase (TS) is a proliferation enzyme and a chemotherapeutic drug target we previously correlated with EMT. Here we report a rather direct role of TS in determining EMT phenotypes in non-small cell lung cancer (NSCLC). TS knockdown and a promoter reporter system revealed the control of TS on EMT, and upstream regulators (HMGA2, HOXC6) and downstream effectors (AXL, SPARC, FOSL1) were identified. In vivo, TS knockdown suppressed lung colonization and metastasis formation in a proliferation-independent manner. Transcriptomic analyses showed a significant enrichment of EMT signature genes in NSCLC patients with high TS levels. These results establish the role of TS as a theranostic NSCLC marker mediating survival, chemo-resistance and EMT, and identifies a regulatory network that could be exploited to target EMT-driven NSCLC.

2020-10-01 | GSE148589 | GEO

Monocyte - neutrophil interplay drives mesenchymal transition in GBM

Project description:Monocyte - neutrophil interplay drives mesenchymal transition in GBM

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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

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

Project description:BackgroundEpithelial-to-mesenchymal transition (EMT) enhances motility, stemness, chemoresistance and metastasis. Little is known about how various pathways coordinate to elicit EMT's different functional aspects in non-small cell lung cancer (NSCLC). Thymidylate synthase (TS) has been previously correlated with EMT transcription factor ZEB1 in NSCLC and imparts resistance against anti-folate chemotherapy. In this study, we establish a functional correlation between TS, EMT, chemotherapy and metastasis and propose a network for TS mediated EMT.MethodsPublished datasets were analysed to evaluate the significance of TS in NSCLC fitness and prognosis. Promoter reporter assay was used to sort NSCLC cell lines in TSHIGH and TSLOW. Metastasis was assayed in a syngeneic mouse model.ResultsTS levels were prognostic and predicted chemotherapy response. Cell lines with higher TS promoter activity were more mesenchymal-like. RNA-seq identified EMT as one of the most differentially regulated pathways in connection to TS expression. EMT transcription factors HOXC6 and HMGA2 were identified as upstream regulator of TS, and AXL, SPARC and FOSL1 as downstream effectors. TS knock-down reduced the metastatic colonisation in vivo.ConclusionThese results establish TS as a theranostic NSCLC marker integrating survival, chemo-resistance and EMT, and identifies a regulatory network that could be targeted in EMT-driven NSCLC.

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p63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

Project description:p63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

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Kras activation in endometrial organoids drives cellular transformation and epithelial-mesenchymal transition

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

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TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

Project description:Epithelial-to-mesenchymal transition (EMT) is a dynamic process that relies on cellular plasticity; an EMT/MET axis is critical for metastatic colonization of carcinomas. Unlike epithelial programming, regulation of mesenchymal programming is not well understood in EMT. Here we describe the first microRNA that enhances exclusively mesenchymal programming. We demonstrate that microRNA-424 is up-regulated early during a TWIST1/SNAI1-induced EMT, and that it causes cells to express mesenchymal genes without affecting epithelial genes, resulting in a mixed/intermediate EMT. Further, microRNA-424 increases motility, decreases adhesion and induces a growth arrest, changes associated with a complete EMT. Patient microRNA-424 levels positively associate with TWIST1/2 and EMT-like gene signatures and is increased in primary tumors versus matched normal breast. However, microRNA-424 is down-regulated in metastases versus matched primary tumors. Correspondingly, microRNA-424 decreases tumor initiation and is post-transcriptionally down-regulated in macrometastases in mice. RNA-seq identified microRNA-424 regulates numerous genes associated with EMT and breast cancer stemness including the novel miR-424 target, TGFBR3, which regulates mesenchymal phenotypes without influencing miR-424 effects on tumor-initiating phenotypes; instead, we show that ERK signaling is critical for such tumor-initiating effects of miR-424. These findings suggest microRNA-424 plays distinct roles downstream of EMT-inducing factors, facilitating earlier stages, but repressing later stages, of metastasis. Examination of mRNA levels in MCF12A human breast cell lines that stably over-expressed miR-424 or an empty vector (EV) control. Each group has three replicates.

2015-02-26 | E-GEOD-54505 | biostudies-arrayexpress

Single-cell transcriptome analysis revealed continuous changes in molecular phenotypes during epithelial-to-mesenchymal transition

Project description:Many genes involved in epithelial-to-mesenchymal transition (EMT) have been identified to date, but mechanisms contributing to the phenotypic diversity and those governing the coupling between the dynamics of epithelial genes and that of the mesenchymal genes are unclear. In this study, we employed single-cell transcriptome analysis to study the gene expression changes during dynamic E-to-M transition. Dose-dependent response to TGFbeta signal suggested that gene expression patterns between E and M states are rather continuous unlike binary switching between two discrete populations. E and M genes can be classified into several subclusters based on expression correlation and it turned out that some E and M genes are mutually exclusive but others are not. Our data suggests that complex and continuous changes in molecular phenotypes occur during EMT at a single-cell level.

2020-01-15 | GSE143607 | GEO

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