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RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

ABSTRACT: RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

PROVIDER: PRJNA756949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15565681_1.fastq.gz	Fastqsanger.gz
	SRR15565681_2.fastq.gz	Fastqsanger.gz
	SRR15565682_1.fastq.gz	Fastqsanger.gz
	SRR15565682_2.fastq.gz	Fastqsanger.gz
	SRR15565683_1.fastq.gz	Fastqsanger.gz

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RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

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Project description:TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

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RNA sequencing of control and DAC-treated CT26 cells.

Project description:PD-1 blockade has demonstrated impressive clinical outcomes in colorectal cancers that have high microsatellite instability. However, the therapeutic efficacy for patients with tumors with low microsatellite instability or stable microsatellites needs further improvement. Here, we have demonstrated that low-dose decitabine could increase the expression of immune-related genes such as major histocompatibility complex genes and cytokine-related genes as well as the number of lymphocytes at the tumor site in CT26 colorectal cancer-bearing mice. A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone. The anti-tumor effect of the PD-1 blockade was enhanced by low-dose decitabine. The results of RNA sequencing and whole-genome bisulfite sequencing of decitabine-treated CT26 cells and tumor samples with microsatellite stability from the patient tumor-derived xenograft model have shown that many immune-related genes, including antigen processing and antigen-presenting genes, were upregulated, whereas the promoter demethylation was downregulated after decitabine exposure. Therefore, decitabine-based tumor microenvironment re-modulation could improve the effect of the PD-1 blockade. The application of decitabine in PD-1 blockade-based immunotherapy may elicit more potent immune responses, which can provide clinical benefits to the colorectal cancer patients with low microsatellite instability or stable microsatellites.

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Project description:Using an optimized analysis data workflow, we identified 3945 genes were upregulated and 510 genes were downregulated in scr senescent cells as compared to scr non-senescent cells. CSE knockdown cells also showed huge differences in gene expression as compared to scr cells in both non-senescent and senescent conditions. For analysis purposes, all samles were used in duplicates.

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Project description:Although membrane-anchored Pd-l1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether Pd-l1 regulate oncogenic signaling pathways in tumor cells remains elusive. In this experiment, to further dissect roles of the K262 residue acetylation for Pd-l1 nuclear function, we profiled RNA expression of WT or K262Q mutant mouse Pd-l1 re-expressed in CT26 KO Pd-l1 cells. Methods: Total RNA fromCT26/Vector, CT26/WT or CT26 Pd-l1 KO cells was purified using Qiagen RNeasy mini kit (Qiagen) according to the manufacturer’s instructions. Library preparation and sequenceing analysis were performed by BGI-Hong Kong Co. Ltd. Conclusions: Our study indicates that Pd-l1 acetylation modification may affect its function in nuclear.

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