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Single-cell Sequencing Analysis Identifies Intratumoral Cell Population in Head and Neck Squamous Cell Carcinoma from 4NQO-induced Mice upon anti-CD276 Therapy

ABSTRACT: Single-cell Sequencing Analysis Identifies Intratumoral Cell Population in Head and Neck Squamous Cell Carcinoma from 4NQO-induced Mice upon anti-CD276 Therapy

PROVIDER: PRJNA692131 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13435850_1.fastq.gz	Fastqsanger.gz
	SRR13435850_2.fastq.gz	Fastqsanger.gz
	SRR13435851_1.fastq.gz	Fastqsanger.gz
	SRR13435851_2.fastq.gz	Fastqsanger.gz
	SRR13435852_1.fastq.gz	Fastqsanger.gz

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Single-cell Sequencing Analysis Identifies Intratumoral Cell Population in Head and Neck Squamous Cell Carcinoma from 4NQO-induced Mice upon anti-CD276 Therapy

Project description:In this study, we aimed to identifies the landscape alterations of intratumoral cell population in HNSCC from 4NQO-induced mice upon anti-CD276 treatment by using single cell sequencing analysis.we characterized the alterations of intratumoral cell population by separating cancer cells and yielded 6 distinct cancer cell subpopulations defined by the transcriptional state of cells and known marker genes, including the sunpopulation with pEMT, stress, typical epithelial differentiation, high cell-cycling, metabolism and immune fetures. In response of CD276 treatment, the frequecey of cells with pEMT, cell cycling and immune features are dcreased as compared to the vehicle control mice.

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PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice

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Therapeutic targeting of BRD4 in head neck squamous cell carcinoma

Project description:The bromodomain and extraterminal family members are epigenetic readers and transcriptional coactivators which are critically involved in various biological processes including tumorigenesis. BRD4 has been increasingly appreciated as a key oncogene and promising anticancer target. Here, we sought to characterize the expression of BRD4 and its tumorigenic roles as well as therapeutic targeting in HNSCC. Expression of BRD4 mRNA and protein was determined by bioinformatics interrogation of public available databases, primary HNSCC samples and 4NQO-induced HNSCC animal model. The tumorigenic roles of BRD4 in HNSCC were evaluated by genetic and pharmacological approach in vitro and in vivo. Therapeutic efficiency of BRD4 targeting by JQ1 was assessed in three preclinical models including xenograft model, 4NQO-induced model and patients-derived xenograft model. Gene candidates responsible for therapeutic effects of JQ1 were identified by transcriptional profiling in HNSCC cells after JQ1 exposure. Significant upregulation of BRD4 was found in primary HNSCC samples and 4NQO-induced HNSCC model. Its overexpression associated with aggressive clinicopathological features and inferior overall and disease-free survival. BRD4 depletion by genetic silencing or pharmacological inhibition impaired cell proliferation, migration and invasion and reduced tumor growth and metastasis in vivo. Transcriptional profiling of HNSCC cells following JQ1 exposure identified hundreds of genes which might mediated its antitumor effects and enriched in cancer-relevant pathways. A novel prognostic risk score derived from JQ1-regualted genes was developed to stratify patients into subgroups with favorable or inferior prognosis. Our findings reveal that BRD4 serves as a novel oncogene driving cancer progression and a robust prognostic biomarker in HNSCC. Therapeutic targeting of BRD4 represents a potent and promising strategy against HNSCC.

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