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Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Feline]

ABSTRACT: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Feline]

PROVIDER: PRJNA1164764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30786182_1.fastq.gz	Fastqsanger.gz
	SRR30786182_2.fastq.gz	Fastqsanger.gz
	SRR30786183_1.fastq.gz	Fastqsanger.gz
	SRR30786183_2.fastq.gz	Fastqsanger.gz
	SRR30786184_1.fastq.gz	Fastqsanger.gz

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Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Feline]

Project description:Oral Squamous Cell Carcinoma (OSCC) is a type of cancer that arises from preneoplastic precursors, which undergo genetic and epigenetic modifications. Lysine-specific demethylase 1 (LSD1) is a key OSCC promoter. LSD1 knockout or pharmacological inhibition in mouse OSCC reversed OSCC preneoplasia in our study. LSD1 inhibition attenuated the cell cycle, immunosuppression and promoted the infiltration of CD45+, TCRß+, CD4+, and CD8+ cells. Next, we tested the clinical candidate LSD1 inhibitor (Seclidemstat) in feline clinically spontaneous natural OSCC and found that it was safe and attenuated the STAT3 network. Mechanistic studies have shown that LSD1 reprograms preneoplasia to promote STAT3 signaling, cell cycle mediator CDK7, and immunosuppressive CTLA4 to OSCC progression. Interestingly, we found that the LSD1 inhibitor (SP2509) attenuated cyclin-dependent kinase 7 (CDK7) phosphorylation at T170 and eukaryotic initiation factor 4 B (Eif4B) phosphorylation at S422. We identified a new mechanism in OSCC preneoplasia that LSD1 promotes STAT3 mediated by CDK7 phosphorylation, leading to overall changes in the tumor microenvironment, leading to immunosuppression and progression to OSCC, which could have applications for understanding the mechanism as well as design strategies to control the progression of preneoplasia to OSCC.

2025-04-23 | GSE277930 | GEO

Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Mice]

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Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Mice]

Project description:Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression [Mice]

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Primary murine embryonic fibroblasts (MEFs): Cdk7 wild type versus Cdk7 KO

Project description:Transcriptional profiling of primary Cdk7lox/lox MEFs comparing Adeno-Cre vs Adeno-GFP infected controls. Samples were obtained 7 days after the Adeno-Cre mediated elimination of Cdk7. Goal was to determine the effects of Cdk7 elimination on RNA polII-mediated transcription. Two-condition experiment, Adeno-Cre vs. Adeno-GFP infected Cdk7lox/lox MEFs. Biological replicates: 10 independent primary MEF preparations.

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Project description:Cyclin-dependent kinase 7 (CDK7) plays a critical role in the general regulation of RNA polymerase II-mediated transcription. However, the absence of selective CDK7 inhibitors has hindered the ability to investigate the consequences of acute and prolonged inhibition of CDK7 under normal and pathological conditions. Here we present the discovery and characterization of the first covalent CDK7 inhibitor, CDK7-IN-1, that has the unprecedented ability to target a unique cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7 amongst the 20 known CDKs. Cancer cell line profiling indicates that a subset of cancer cell lines, including T-cell acute lymphoblastic leukemia (T-ALL), exhibit 100-fold greater sensitivity to CDK7-IN-1 over other tumor and normal cell lines. Genome-wide expression analysis in Jurkat T-ALL indicates that CDK7-IN-1 disproportionally affects RUNX1 as well as other components of the TAL1 transcriptional network and its targets, downregulating key regulators of transcription and apoptosis critical for the T-ALL state. These oncogenes are encoded by short-lived mRNA transcripts, are associated with super-enhancers, and exhibit a strong dependency on continuous transcription for sustained expression. Therefore, pharmacological modulation of CDK7 kinase activity may define a method for the identification and treatment of tumor types exhibiting extreme dependencies on transcription for maintenance of the oncogenic state. Jurkat, MM1S, Loucy, and HeLa (WT and Dox-inducible CDK7 mutant) cells were treated with various drugs including a covalent inhibitor of CDK7 (CDK7-IN-1), a reversible inhibitor of CDK7 (CDK7-IN-1), Flavopiridol, Actinomycin D, and DMSO controls. Replicates are annotated.

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