Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immune suppressive effects of radiotherapy promote metastasis

ABSTRACT: Immune suppressive effects of radiotherapy promote metastasis

PROVIDER: PRJNA960856 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24279223.fastq.gz	Fastqsanger.gz
	SRR24279224.fastq.gz	Fastqsanger.gz
	SRR24279225.fastq.gz	Fastqsanger.gz
	SRR24279226.fastq.gz	Fastqsanger.gz
	SRR24279227.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Immune suppressive effects of radiotherapy promote metastasis

Project description:We report the transcriptomic profile of immune cells for lungs of tumor bearing mice of which tumor received radiation (20Gy)

2024-02-16 | GSE230368 | GEO

YTHDF2 inhibition potentiates radiotherapy by reprogramming suppressive myeloid cells

Project description:YTHDF2 inhibition potentiates radiotherapy by reprogramming suppressive myeloid cells

| PRJNA850417 | ENA

Glucocorticoids Promote Breast Cancer Metastasis

Project description:Glucocorticoids Promote Breast Cancer Metastasis

| PRJNA513860 | ENA

YTHDF2 inhibition potentiates radiotherapy by reprogramming suppressive myeloid cells [scRNA-Seq]

Project description:RNA N6-methyladenosine (m6A) modification is implicated in cancer progression. However, the impact of m6A on the antitumor effects of radiotherapy and the related mechanisms are unknown. Here we show that ionizing radiation (IR) induces immunosuppressive myeloid-derived suppressor cell (MDSC) expansion and YTHDF2 expression in both murine models and humans. Following IR, loss of Ythdf2 in myeloid cells augments antitumor immunity and overcomes tumor radioresistance by altering MDSC differentiation and inhibiting MDSC infiltration and suppressive function. The remodeling of the landscape of MDSC populations by local IR is reversed by Ythdf2 deficiency. IR-induced YTHDF2 expression relies on NF-κB signaling; YTHDF2 in turn leads to NF-κB activation by directly binding and degrading transcripts encoding negative regulators of NF-κB signaling, resulting in an IR-YTHDF2-NF-κB circuit. Pharmacological inhibition of YTHDF2 overcomes MDSC-induced immunosuppression and improves combined IR and/or anti-PD-L1 treatment. Thus, YTHDF2 is a promising target to improve radiotherapy (RT) and RT/immunotherapy combinations.

2023-04-28 | GSE206378 | GEO