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Irinotecan activates anti-tumor immunity in CT26 subcutaneous tumors

ABSTRACT: Topoisomerase I (Top1) is a classical drug target for anticancer therapy, but its role in immune signaling in cancer cells remain unclear. Here, we aimed to explore the possible role and mechanism of Irinotecan (CPT-11) in anti-tumor immunity.

ORGANISM(S): Mus musculus

PROVIDER: GSE245431 | GEO | 2025/10/16

REPOSITORIES: GEO

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Irinotecan activates anti-tumor immunity in CT26 tumor cells

Project description:Topoisomerase I (Top1) is a classical drug target for anticancer therapy, but its role in immune signaling in cancer cells remain unclear. Here, we aimed to explore the possible role and mechanism of Irinotecan (CPT-11) in anti-tumor immunity.

2025-10-12 | GSE245337 | GEO

Irinotecan activates anti-tumor immunity in HCT116 tumor cells

2025-10-18 | GSE245809 | GEO

Topoisomerase I cleavage complexes preferentially down-regulate ubiquitin- and RNA degradation-related transcripts in relationship to gene length, exon-intron junctions and p53-dependent up-regulation of miR-142-3p [miRNA]

Project description:DNA topoisomerase I (Top1) is required for transcription as it relaxes positive and negative supercoils by forming transient Top1 cleavage complexes (Top1cc) up- and down-stream of transcription complexes. However, Top1cc can also be trapped by endogenous DNA lesions and by camptothecin (CPT) and its anticancer derivatives, which results in transcription blocks. Here, we undertook a genome-wide analysis of the effects of CPT on gene expression at exon resolution. We tested the impact of Top1 inhibition on miRNA expression at the genome-wide level in human colon carcinoma HCT116. The miRNA of cells treated with camptothecin (CPT) for were measured at several timepoints with Agilent Human miRNA Microarray V3 (8x15K).

2013-04-17 | E-GEOD-37357 | biostudies-arrayexpress

2013-04-17 | GSE37357 | GEO

Transcription poisoning by topoisomerase I is controlled by gene length, splice sites and miR-142-3p

2013-04-17 | GSE37352 | GEO

Transcription poisoning by topoisomerase I is controlled by gene length, splice sites and miR-142-3p

Project description:DNA topoisomerase I (Top1) is required for transcription as it relaxes positive and negative supercoils by forming transient Top1 cleavage complexes (Top1cc) up- and down-stream of transcription complexes. However, Top1cc can also be trapped by endogenous DNA lesions and by camptothecin (CPT) and its anticancer derivatives, which results in transcription blocks. Here, we undertook a genome-wide analysis of the effects of CPT on gene expression at exon resolution. We tested the impact of Top1 inhibition on gene expression at the genome-wide level in human colon carcinoma HCT116 and human breast carcinoma MCF7 cells. The RNA of cells treated with camptothecin (CPT) for various times was analyzed with Affy Exon array (GeneChip Human Exon 1.0 ST array). Moreover, we tested the impact of Top1 down-regulation on gene expression at the genome-wide level in human colon carcinoma HCT116 cells. The RNA of cells treated transfected with a Top1 siRNA was analyzed with Affy Exon array (GeneChip Human Exon 1.0 ST array).

2013-04-17 | E-GEOD-37352 | biostudies-arrayexpress

Transcription profiling of topoisomerase I inhibitor irinotecan (CPT-11) sensitive, resistant, and reverted human neuroblastomas

Project description:We have established a neuroblastoma model resistant in vivo to the topoisomerase I inhibitor irinotecan (CPT-11, Camptothecin-11, CAMPTOSAR®) in order to study resistance to these agents acquired in a therapeutic setting. Common mechanisms of resistance were not involved in this model and we thus explored the gene expression signature associated with resistance by comparing the transcriptomes of sensitive, resistant, and reverted tumours using high-throughput DNA microarrays.

2008-01-26 | E-TABM-211 | biostudies-arrayexpress

Curcumin reverses irinotecan-acquired resistance in colorectal cancer cells: insights from whole transcriptomic data

Project description:To investigate the key mechanisms underlying the acquisition of irinotecan resistance in colorectal cancer cells and the reversal of this resistance by curcumin, we utilized whole-genome microarray expression profiling as a discovery tool to identify the signaling networks involved. Resistance acquisition led to dysregulation of genes associated with irinotecan resistance, including TOP1, drug-metabolizing enzymes (CYPs and UGTs), and efflux transporters (ABCs), while also affecting the extression of 53 genes involed in proliferation and 33 in cell motility. Curcumin treatment significantly modulated 3,901 genes (FC >|±2|), inducing apoptosis, reducing proliferation, and inhibiting migration. Curcumin also enhanced sensitivity to irinotecan, by upregulating TOP1 and inhibiting 18 CYPs, 4 UGTs, and 20 ABCs, including those upregulated in irinotecan-resistant cells.

2025-02-03 | GSE288308 | GEO

Irinotecan activates anti-tumor immunity in CT26 tumor cells

Project description:Irinotecan activates anti-tumor immunity in CT26 tumor cells

| PRJNA1027843 | ENA

Expression data from Irinotecan resistant LoVo cells comapred to parental LoVo cells

Project description:Irinotecan, an analogue of camptothecin, is frequently used in combination with various anticancer drugs or as a single agent in treatment of colorectal cancer. But drug resistance of tumor is still a major obstacle to overcome for the success of cancer treatment. In this study, We established chronic irinotecan resistant cell line for new marker to increase the sensitivity to irinotecan and investigated gene expression profiles of the irinotecan-resistant colorectal cancer cell line.

2014-07-18 | GSE59501 | GEO

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