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CDK10 suppresses nucleic acid sensors-mediated antitumor immunity [scRNA-Seq]

ABSTRACT: Cdk10 knockout significantly reduced CT26 tumor growth in immunocompetent BALB/c WT mice. To investigate how Cdk10 influences the tumor immune microenvironment in vivo, we performed single-cell RNA sequencing (scRNA-seq) on WT and Cdk10 KO CT26 tumors derived from immunocompetent BALB/c mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE287052 | GEO | 2025/10/27

REPOSITORIES: GEO

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CDK10 suppresses nucleic acid sensors-mediated antitumor immunity [RNA-Seq]

Project description:Cdk10 knockout significantly reduced CT26 tumor growth in immunocompetent BALB/c WT mice.To elucidate the molecular mechanisms by which Cdk10 suppresses anti-tumor immunity, we conducted transcriptomic analyses on WT and Cdk10 KO CT26 cells

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CDK10 suppresses nucleic acid sensors-mediated antitumor immunity [CRISPR screening]

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2024-03-12 | E-MTAB-13823 | biostudies-arrayexpress

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RNA-seq of CT26 subcutaneous tumors expressing control or Gna13 targeting sgRNAs

Project description:CT26 cells expressing lentiviral Cas9 and sgRNAs targeting either control or Gna13 were transplanted into immunocompetent BALB/c mice. Tumors were harvested and processed for RNA-seq

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Project description:Recently, attenuated Semliki Forest virus vector VA7 completely eliminated type I interferon (IFN) unresponsive human U87 glioma xenografts while IFN responsive mouse GL261 and CT-2A gliomas proved refractory to the oncolytic virotherapy. Here we describe in two clones of a well established Balb/c mouse tumor cell line, CT26 murine colon carcinoma, diametrically opposed IFN responsiveness and sensitivity to oncolytic virus. Both CT26WT and CT26LacZ clones secreted biologically active type I IFN in vitro upon infection but virus replication was self-limiting only in CT26WT cells. Total transcriptome sequencing (RNA-Seq) and western blotting experiments revealed that in sharp contrast to CT26LacZ cells, CT26WT cells had strong constitutive expression of 56 different genes associated with pattern recognition and type I interferon signaling pathways, spanning two reported anti-RNA virus gene signatures and22 genes that have been reported to have direct anti-Alphaviral activity. Correspondingly, only CT26LacZ tumors were infectable in vivo, resulting in rapid central necrosis of the tumors by 96 hours post infection and complete tumor eradication both in immunocompetent and in SCID mice. CT26LacZ tumor eradication by oncolysis induced 100% protective immunity against homologous CT26LacZ challenge but only 50% protection against heterologous CT26WT challenge, indicating LacZ immune dominance over shared antigens. We believe the two clone CT26 system described herein constitutes a challenging yet realistic model for clonally and immunologically heterogeneous cancer where a strong therapy efficacy bias toward sensitive tumor subpopulations might falsely predict therapeutic success on a broad patient scale highlighting the necessity of successful pre-screening for responsive tumors. RNA-Seq in CT26 tumor cell line

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