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DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden'

ABSTRACT: DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden'

PROVIDER: PRJNA1203199 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31831920.fastq.gz	Fastqsanger.gz
	SRR31831921.fastq.gz	Fastqsanger.gz
	SRR31831922.fastq.gz	Fastqsanger.gz
	SRR31831923.fastq.gz	Fastqsanger.gz
	SRR31831924.fastq.gz	Fastqsanger.gz

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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

Project description:High tumor mutational burden (TMB) is a predictive biomarker for the responsiveness of cancer to immune checkpoint inhibitor therapy that indicates whether immune cells can sufficiently recognize cancer cells as non-self. However, about 30% of all cancers from The Cancer Genome Atlas are classified as immune-desert tumors lacking T cell infiltration despite high TMB. Since the underlying mechanism of these immune-desert tumors has yet to be unraveled, there is a pressing need to transform such immune-desert tumors into immune-inflamed tumors and thereby enhance their responsiveness to anti-PD1 therapy. Here, we present a systems framework for identifying immuno-oncotargets, based on analysis of gene regulatory networks, and validating the effect of these targets in transforming immune-desert into immune-inflamed tumors. In particular, we identify DEAD-box helicases 54 (DDX54) as a master regulator of immune escape in immune-desert lung cancer with high TMB, and show that knockdown of DDX54 can increase immune cell infiltration and lead to improved sensitivity to anti-PD1 therapy.

2025-03-19 | GSE268555 | GEO

DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [Xenium]

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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [miRNA-Seq]

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DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

Project description:DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

| PRJNA1203202 | ENA

DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

Project description:DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

| PRJNA1221574 | ENA

DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

Project description:DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

| PRJNA1117802 | ENA

DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [bulk RNA-seq]

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Characterization of tumor mutational burden in LKB1 mutant lung tumors

Project description:Inactivating mutations in LKB1/STK11 are present in ~20% of non-small cell lung cancers (NSCLC) and portend poor response to anti-PD-1 immunotherapy in patients and genetically engineered mouse model (GEMMs). Here, we sought to uncover the basis for immunotherapy resistance of these tumors and to define strategies that overcome this barrier. Whereas high tumor mutational burden (TMB) often correlates with response to anti-PD1 treatment, we found that LKB1-deficient NSCLCs from non-smokers and GEMMs exhibited striking elevations in nonsynonymous mutations compared to LKB1 wildtype tumors. Correspondingly, LKB1 mutant NSCLC cell lines showed defects in both replication dependent and independent double-strand DNA break (DSB) repair, which were reversed upon LKB1 re-expression.

2021-03-17 | GSE137244 | GEO

miRNA expression between CD4+PD1+ and CD4+PD1- T cells

Project description:Recent success in cancer immunotherapy has come from the blockade of inhibitory receptors on T cells, such as programmed cell death-1, which can induce a state of T cell exhaustion upon constant antigen stimulation. Understanding miRNA regulation of PD1 can be useful to discover miRNAs for use in therapy or as prognostic markers in various diseases including cancer, autoimmunity and transplantation. We used microarrays to discover global miRNA expression changes upon PD1 upregulation and identified miRNAs that are both up- and down-regulated. B16F10 cells were injected subcutaneously into C57BL/6 mice and 16 days later CD4+PD1+ and CD4+PD1- were sorted from the lymph nodes and spleen for RNA extraction and hybridization on Affymetrix miRNA array.

2015-08-01 | E-GEOD-65208 | biostudies-arrayexpress

DDX54 regulates transcriptome dynamics during DNA damage response, DDX54 BioID

Project description:The cellular response to genotoxic stress is a well-characterized network of DNA surveillance pathways. The contribution of posttranscriptional gene regulatory networks to the DNA damage response (DDR) has not been extensively studied. Here, we systematically identified RNA-binding proteins differentially interacting with polyadenylated transcripts upon exposure of human breast carcinoma cells to ionizing irradiation (IR). Interestingly, more than 260 proteins showed increased binding to poly(A) RNA in IR-exposed cells and were comprised of many nucleolar proteins. The functional analysis of DDX54, a candidate genotoxic stress responsive RNA helicase, revealed that DDX54 is an immediate-to-early DDR regulator required for the splicing efficacy of its target IR-induced pre-mRNAs. Upon IR exposure, DDX54 acts by increased interaction with a well defined class of pre-mRNAs which harbor introns with weak acceptor splice sites, as well as by protein-protein contacts within components of U2 snRNP and spliceosomal B complex, resulting in lower intron retention and higher processing rates of its target transcripts. Since DDX54 promotes survival after exposure to IR its expression and/or mutation rate may impact DDR-related pathologies. Our work indicates the relevance of many uncharacterized RBPs potentially involved in the DDR.

2017-06-12 | PXD005191 | Pride

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