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Cancer-associated exportin-6 upregulation inhibits the transcriptional repressive and anticancer effects of nuclear profilin-1

ABSTRACT: Cancer-associated exportin-6 upregulation inhibits the transcriptional repressive and anticancer effects of nuclear profilin-1

PROVIDER: PRJNA603508 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10980118_1.fastq.gz	Fastqsanger.gz
	SRR10980118_2.fastq.gz	Fastqsanger.gz
	SRR10980119_1.fastq.gz	Fastqsanger.gz
	SRR10980119_2.fastq.gz	Fastqsanger.gz
	SRR10980120_1.fastq.gz	Fastqsanger.gz

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Cancer-associated exportin-6 upregulation inhibits the transcriptional repressive and anticancer effects of nuclear profilin-1

Project description:Aberrant expression of nuclear transporters and altered subcellular localization of their cargo proteins are increasingly recognized as drivers and therapeutic targets of cancer. Here, we report that exportin-6, a nuclear exporter specific for actin/profilin-1, is upregulated in a broad range of cancers and associated with poor prognosis. Exportin-6 loss triggers antitumor effects in breast cancer cells in a profilin-1-dependent fashion. Nuclear profilin-1 interacts with the Super Elongation Complex (SEC), a positive transcriptional regulator of pro-cancer genes including MYC. Exportin-6 loss, by increasing nuclear profilin-1, inhibits SEC-dependent transcription and sensitizes breast cancer cells to inhibition of BET domain proteins. Thus, exportin-6 upregulation is a previously unrecognized cancer addiction that reduces the transcriptional inhibitory and anticancer activities of nuclear profilin-1.

2021-04-07 | GSE144372 | GEO

Cancer-associated exportin-6 upregulation inhibits the transcriptionally repressive and anticancer effects of nuclear profilin-1.

Project description:Aberrant expression of nuclear transporters and deregulated subcellular localization of their cargo proteins are emerging as drivers and therapeutic targets of cancer. Here, we present evidence that the nuclear exporter exportin-6 and its cargo profilin-1 constitute a functionally important and frequently deregulated axis in cancer. Exportin-6 upregulation occurs in numerous cancer types and is associated with poor patient survival. Reducing exportin-6 level in breast cancer cells triggers antitumor effects by accumulating nuclear profilin-1. Mechanistically, nuclear profilin-1 interacts with eleven-nineteen-leukemia protein (ENL) within the super elongation complex (SEC) and inhibits the ability of the SEC to drive transcription of numerous pro-cancer genes including MYC. XPO6 and MYC are positively correlated across diverse cancer types including breast cancer. Therapeutically, exportin-6 loss sensitizes breast cancer cells to the bromodomain and extra-terminal (BET) inhibitor JQ1. Thus, exportin-6 upregulation is a previously unrecognized cancer driver event by spatially inhibiting nuclear profilin-1 as a tumor suppressor.

| S-EPMC8006859 | biostudies-literature

Expression data from allergic patients to profilin

Project description:Prevalence and severity of allergic diseases have increased worldwide. To date, respiratory allergy phenotypes are not fully characterized and, along with inflammation progression, treatment is increasingly complex and expensive. Profilin sensitization constitutes a good model to study the progression of allergic inflammation. We have used microarrays to understand the underlying mechanisms of severe profilin-mediated reactions using a model that includes patients with different levels of sensitization to profilin (non-allergic, mild, moderate and severe)

2018-05-22 | GSE114707 | GEO

The effects of novel adjuvant complex and CpG ODN on host immune response to recombinant Eimeria profilin vaccine

Project description:This study investigated the ability of two novel adjuvant formulations, QCDC (Quil A/cholesterol/DDA/Carbopol) and QCDCR (QCDC/Bay R1005), in combination with a recombinant profilin vaccine, to modulate host protective immunity and to alter new gene expression during experimental avian coccidiosis. Four-condition experiment, Profilin only vs. Non-vaccination, Profilin only vs. Co-vaccination of QCDC plus profilin, Profilin only vs. Co-vaccination of QCDCR plus profilin, Biological replicates: 2 profilin only replicates, 2 Non-vaccination replicates, 2 QCDC plus profilin replicates, 2 QCDCR plus profilin replicates with dye-switching.

2010-10-28 | E-GEOD-24966 | biostudies-arrayexpress

Effect of Exportin-5 expression on Mouse fibroblasts in cell cycle re-entry phase

Project description:To analyze the effect of Exportin-5 expression on the MEF cells in cell cycle re-entry phase, we have employed whole genome microarray expression profiling on the MEF cells in cell cycle re-entry phase with and without down regulation of Exportin-5 gene. Mouse MEF cells were transfected with 60nM of siRNA targeting either Exportin-5 or negative control, and incubated for 12 hours. After incubation, cells were starved with DMEM containing 0.2% FCS for 48 hours and re-fed with DMEM containing 20%FCS for 24 hours, along with second siRNA transfection. Two independant expreiments were preformed.

2013-01-01 | E-GEOD-25498 | biostudies-arrayexpress

Potential binding partners of profilin protein from Leishmania donovani

Project description:For identifying potential ligands of Leishmania profilin (LdPfn) protein, full length profilin was cloned and expressed with GST tag. Only GST tag protein was used as a negative control. Employing pull down assay and with the help of LC-MS, the potential binding partners of profilin protein in Leishmania promastigotes were detected.

2022-03-10 | PXD026036 | Pride

Exportin 1 inhibition prevents neuroendocrine transformation through SOX2 downregulation in lung and prostate cancers [RNA-seq]

Project description:In lung and prostate adenocarcinomas, neuroendocrine (NE) transformation to an aggressive derivative resembling small cell lung cancer (SCLC) is associated with poor prognosis. We previously described dependency of SCLC on the nuclear transporter exportin 1. Here we explored the role of exportin 1 in NE transformation. We observed upregulated exportin 1 in lung and prostate pre-transformation adenocarcinomas. Exportin 1 was induced upregulated following genetic inactivation of TP53 and RB1 in lung and prostate adenocarcinoma cell lines, accompanied by increased sensitivity to the exportin 1 inhibitor selinexor in vitro. Exportin 1 inhibition prevented NE transformation and extended response to targeted therapies in both lung anddifferent TP53/RB1-inactivated prostate adenocarcinoma xenograft models that acquire NE features upon treatment with the AR inhibitor enzalutamide, and extended response to the EGFR inhibitor osimertinib in a lung cancer transformation patient-derived xenograft (PDX) model exhibiting combined adenocarcinoma/SCLC histology. Ectopic SOX2 expression restored the enzalutamide-promoted NE transformationNE phenotype on adenocarcinoma-to-NE transformation xenograft models despite selinexor treatment. Selinexor sensitized NE-transformed lung and prostate small cell carcinoma PDXs tumors after NE transformation to standard cytotoxics. Together these data nominate exportin 1 inhibition as a novel potential therapeutic approach target to constrain lineage plasticity and prevent or treat NE transformation in lung and prostate adenocarcinoma.

2023-07-12 | GSE237072 | GEO

Exportin 1 inhibition prevents neuroendocrine transformation through SOX2 downregulation in lung and prostate cancers [ATAC-seq]

2023-07-12 | GSE237071 | GEO

Effect of Exportin-5 expression on Mouse fibroblasts in cell cycle re-entry phase

2013-01-01 | GSE25498 | GEO

Expression data from allergic patients to profilin

Project description:Expression data from allergic patients to profilin

| PRJNA472340 | ENA