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ALPN-202 induces a more potent anti-tumor T cell response in MC38/hPD-L1 tumors than PD-L1 blockade alone

ABSTRACT: ALPN-202 induces a more potent anti-tumor T cell response in MC38/hPD-L1 tumors than PD-L1 blockade alone

PROVIDER: PRJNA676031 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13023900.fastq.gz	Fastqsanger.gz
	SRR13023901.fastq.gz	Fastqsanger.gz
	SRR13023902.fastq.gz	Fastqsanger.gz
	SRR13023903.fastq.gz	Fastqsanger.gz
	SRR13023904.fastq.gz	Fastqsanger.gz

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ALPN-202 induces a more potent anti-tumor T cell response in MC38/hPD-L1 tumors than PD-L1 blockade alone

Project description:Purpose: Use RNA-seq to characterize the anti-tumor immune response induced by ALPN-202 and compare to that of anti-PD-L1 treatment alone. Methods: mRNA was isolated from MC38/hPD-L1 tumors 72 hours after a single dose of ALPN-202 (n=4), anti-PD-L1 mAb (durvalumab) (n=4), or Fc control (n=4). Results: ALPN-202 treatment resulted in elevated expression of multiple T cell, NK cell, myeloid cell genes. Additionally, there was a strong increase in genes commonly associated with a proinflammatory response including cytokines, chemokines and surface markers. Conclusions: ALPN-202 treatment resulted in a strong anti-tumor immune response that was more potent than that generated by blockade of PD-L1 alone.

2022-02-10 | GSE161244 | GEO

Single-cell RNAseq of CD45 positive cells in MC38 tumors - Primary irradiated tumors and secondary non-irradiated tumors - Concurrent treatment with anti-PD-L1

Project description:Primary irradiated MC38 tumors and secondary MC38 non-irradiated tumors. Subcutaneous MC38 tumors in C57BL/6 mice Concurrent treatment with anti-PD-L1.

2023-10-15 | E-MTAB-13389 | biostudies-arrayexpress

Macrophage phenotype in anti-PD-L1 treated MC38 tumors

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ATAC-Seq analysis of MC38 colon carcinoma cells and MC38 Bap1-knockout cells

Project description:Genome-wide measurements of chromatin accessibility in MC38 colon carcinoma cells and MC38 Bap1-knockout cells.

2025-07-06 | E-MTAB-10593 | biostudies-arrayexpress

The microARN-202 (miR-202) controls female fecundity by regulating oogenesis in medaka

Project description:In fish, female fecundity is tightly linked to the proper completion of oogenesis that takes place in the ovary. These cellular processes have been shown to involve both endocrine and intra-ovarian factors. However, the role of small non-coding miRNAs remains largely unknown. Here, we analyzed the role of miR-202, a miRNA specifically expressed in the vertebrate gonads. We first used fluorescent in situ hybridization to determine the precise cellular expression of miR-202 in the medaka ovary. We then generated a mutant fish line (using CRISPR/Cas9 technology) to determine its role in female fecundity and oogenesis. We performed quantitative image analyses to analyze cellular modifications and a genome-wide transcriptomic approach to analyze gene expression modifications. Our results show that miR-202-5p is predominantly expressed in granulosa cells. In addition, mutant females display a drastically reduced fecundity. Our cellular and molecular analyses of ovaries from mutant females indicate that miR-202 deficiency impairs the early steps of oogenesis/folliculogenesis, which ultimately reduce female fecundity. This provides the first functional evidence that miR-202 is necessary for the female reproductive success, in particular the female fecundity, and shed new light on the regulatory mechanisms that control the early steps of follicular development.

2018-08-27 | GSE111388 | GEO

Whole exome sequencing of MC38 colon carcinoma cells and MC38 Bap1-knockout cells

Project description:In recent years,Bap1 has been reported to be involved in the process of tumorigenesis. Bap1 gene mutations frequently occur in tumors such as uveal melanoma, mesothelioma, and kidney cancer. In our study,we found that Bap1 deletion in MC38 colon carcinoma cells can promote anti-tumor immune response. To investigate how the genetic mutational landscape,whole exome sequencing of MC38 colon carcinoma cells and MC38 Bap1-knockout cells were performed.

2025-06-30 | E-MTAB-10584 | biostudies-arrayexpress

Immunopeptidome on MC38 Cell line

Project description:PTM – driven antigenicity – immunopeptidome of MC38 cell line

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Transcriptomic profiling of CRISPR-Cas9 knockout of RAD51D, LIMCH1, and BRD9 in MC38 colorectal cancer cells reveals regulation of PD-L1 expression

Project description:Programmed death-ligand 1 (PD-L1) expression in tumor cells plays a critical role in regulating anti-tumor immune responses and determining the efficacy of immune checkpoint blockade therapy. Previous studies have suggested that multiple genes are associated with PD-L1 expression in colorectal cancer, but the underlying regulatory mechanisms remain incompletely understood. In this study, we investigated the transcriptional consequences of knocking out three candidate genes, RAD51D, LIMCH1, and BRD9, which were previously identified to be associated with PD-L1 expression in colorectal cancer. Using the murine colorectal cancer cell line MC38, we generated CRISPR-Cas9–mediated knockout cell lines targeting each gene and performed RNA sequencing to characterize the global transcriptomic alterations. Our results revealed that RAD51D deficiency led to activation of the JAK1–STAT1 signaling pathway, accompanied by increased expression of JAK1, STAT1, and IRF1, which are known transcriptional regulators of PD-L1. Consistently, PD-L1 transcription was upregulated following RAD51D knockout. Similar transcriptomic analyses were performed for LIMCH1 and BRD9 knockout cells to explore their potential regulatory roles in PD-L1 expression and tumor immune signaling. This dataset provides a comprehensive transcriptomic resource for understanding how these genes regulate PD-L1 expression and immune-related signaling pathways in colorectal cancer cells, and may facilitate further studies on the molecular mechanisms underlying tumor immune evasion and responses to immune checkpoint blockade.

2026-03-18 | GSE324386 | GEO

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2021-05-21 | GSE169157 | GEO

PD-L1 regulates dendritic cell ferroptosis during immunogenic chemotherapy [scRNA-seq]

Project description:Dendritic cells (DCs) express high levels of PD-L1 in the tumor microenvironment and draining lymph nodes. Here, we explore the roles of PD-L1 signaling during immunogenic chemotherapy. DC-conditional PD-L1 knockout mice were inoculated with MC38-OVA tumors and treated with doxorubicin. T cells were isolated from draining lymph node for single cell RNA sequencing.

2024-09-23 | GSE223509 | GEO

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