Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of HeLa cell transcriptome changes induced by IDO1-metabolism

ABSTRACT: Analysis of HeLa cell transcriptome changes induced by IDO1-metabolism

PROVIDER: PRJNA728450 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14475317_1.fastq.gz	Fastqsanger.gz
	SRR14475317_2.fastq.gz	Fastqsanger.gz
	SRR14475318_1.fastq.gz	Fastqsanger.gz
	SRR14475318_2.fastq.gz	Fastqsanger.gz
	SRR14475319_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Analysis of HeLa cell transcriptome changes induced by IDO1-metabolism

Project description:We analyzed the mRNA changes iduced by treatment with IFNγ in the presence of the IDO1 inhibitors (indoximod, epacadostat and BMS986205) in wt and IDO1 ko HeLa cells.

2022-01-11 | GSE174116 | GEO

PABPC1L promotes tryptophan metabolism and immune suppression by stabilizing IDO1 in renal cell carcinoma

Project description:The tumor microenvironment (TME) in renal cell carcinomas (RCC) is marked by substantial immunosuppression and immune resistance though highly infiltrated by T cells. There is an urgent need to elucidate tumor immune evasion and to develop novel therapeutic target to boost the efficacy of immune checkpoint blockade (ICB) in RCC. Our study uncovers a mechanism wherein the polyadenylate-binding protein PABPC1L modulates indoleamine2, 3dioxygenase1 (IDO1), a prospective candidate for immunotherapy. PABPC1L, markedly upregulated in RCC, correlates with unfavorable prognosis and resistance to ICB. Overexpressed PABPC1L bolsters tryptophan metabolism and induces T-cell dysfunction by stabilizing IDO1. Conversely, silencing PABPC1L diminishes IDO1 expression, mitigates cytotoxic T-cell suppression, and enhances responsiveness to anti-PD-1 therapy. Our findings underscore PABPC1L's crucial role in facilitating immune evasion in RCC, making it a potential addition to ICB therapy.

2024-02-14 | GSE241871 | GEO

PABPC1L promotes tryptophan metabolism and immune suppression by stabilizing IDO1 in renal cell carcinoma [RIP-seq]

2024-02-14 | GSE255448 | GEO

Analysis of HeLa cell transcriptome changes induced by Indole-3-pyruvate and mIL4i1

Project description:We analyzed the mRNA changes induced by Indole-3-pyruvate (I3P) and WT or K351A mutant mIL4i1 in HeLa cells.

2021-03-07 | GSE167136 | GEO

Transcriptional changes induced by ADH5 knocking out in HeLa cells.

Project description:Transcriptional changes induced by ADH5 knocking out in HeLa cells.

| PRJNA868944 | ENA

Analysis of HeLa cell transcriptome changes induced by Indole-3-pyruvate and mIL4i1

Project description:Analysis of HeLa cell transcriptome changes induced by Indole-3-pyruvate and mIL4i1

| PRJNA703053 | ENA

PABPC1L promotes tryptophan metabolism and immune suppression by stabilizing IDO1 in renal cell carcinoma

Project description:PABPC1L promotes tryptophan metabolism and immune suppression by stabilizing IDO1 in renal cell carcinoma

| PRJNA1010378 | ENA

An adverse tumor-protective effect of IDO1 inhibition

Project description:Indoleamine 2, 3-dioxygenase 1 (IDO1) is a metabolic enzyme catalyzing the conversion of the essential amino acid tryptophan to kynurenine. It is induced by IFNg and its expression is linked to poor prognosis across various cancer types. T cells are particularly sensitive to IDO1-dependent tryptophan deprivation in the tumor microenvironment, leading to tumor immune resistance. Therefore, IDO1 inhibitors, such as epacadostat, have been developed, aiming to restore T cell antitumor activity. However, a recent phase III trial assessing the clinical benefit of epacadostat with the PD-1 antibody pembrolizumab in melanoma failed. This prompted us to study the role of IDO1, and the effect of its inhibition, on tumor cells that are under IFNg treatment and T cell attack. We showed that IDO1-mediated tryptophan depletion contributes to the anti-tumor effect of CD8 T cells. Thus, while epacadostat expectedly replenished tryptophan -the desired effect-, this led to adverse protection of melanoma cells from T cell-derived IFNg. RNA sequencing and ribosome profiling of (patient-derived) melanoma cell lines revealed that IFNg caused general protein translation shut down, which was reversed by IDO1 inhibition. Impaired translation was accompanied by an amino acid deprivation-dependent stress response driving ATF4high and MITFlow transcriptomic signatures, which was also observed in melanoma patient tumors. Downregulation of MITF in tumors and PDX- derived cell lines upon treatment was strongly predictive of response to response, to checkpoint blockade-treatment and IFNg, respectively. Conversely, MITF restoration in cultured tumor cells caused T cell resistance. These results highlight the critical role of tryptophan in the melanoma response to T cell-derived IFNg, uncovering an unexpected negative consequence of IDO1 inhibition.

2023-01-16 | GSE198460 | GEO

DNA Changes That Affect Vitamin D Metabolism in Patients With Colorectal Cancer Receiving Vitamin D Supplements

Project description:RATIONALE: Studying samples of blood from patients with cancer in the laboratory may help doctors learn more about changes that occur in DNA and identify biomarkers related to cancer. PURPOSE: This clinical trial is studying changes in DNA that affect vitamin D metabolism in patients with colorectal cancer receiving vitamin D supplements.

| 2045801 | ecrin-mdr-crc

Sex differences in FGF21-induced changes in hepatic metabolism

Project description:Sex differences in FGF21-induced changes in hepatic metabolism

| PRJNA867142 | ENA