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Recurrent human papillomavirus-related head and neck cancer undergoes metabolic re-programming and is driven by oxidative phosphorylation

ABSTRACT: Recurrent human papillomavirus-related head and neck cancer undergoes metabolic re-programming and is driven by oxidative phosphorylation

PROVIDER: PRJNA698536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13594900_1.fastq.gz	Fastqsanger.gz
	SRR13594900_2.fastq.gz	Fastqsanger.gz
	SRR13594901_1.fastq.gz	Fastqsanger.gz
	SRR13594901_2.fastq.gz	Fastqsanger.gz
	SRR13594902_1.fastq.gz	Fastqsanger.gz

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Recurrent human papillomavirus-related head and neck cancer undergoes metabolic re-programming and is driven by oxidative phosphorylation

Project description:Human papillomavirus (HPV) infection drives the development of some head and neck cancer squamous cell carcinomas (HNSC). Although these tumors are sensitive to treatment, ~10% of patients fail therapy. However, the mechanisms that underlie treatment failure remain unclear. Here, we assessed the transcriptional profiles of 10 paired primary and subsequent recurrent HPV-related oropharyngeal squamous cell carcinomas (OPSCCs) using an exome-capture hybrid RNA sequencing assay. Principal componenent analysis using the expression data from the top 500 most variable genes revealed that 29.3% of the variance was aassociated with tumor status (i.e., primary vs recurrent tumor). Four of the primary/recurrent tumor pairs demonstrated greater clustering based on the patient of origin rather than the tumor status (primary vs recurrent). Additionally, two of the recurrences were distant, two were local, and the remaining six were regional. The recurrent tumors did not cluster necessairly based on site of recurrence. Unsupervised heirarchical clustering of the top 500 most variable genes revealed a correlation between recurrent tumors and metabolic gene expression while the primary tumors demonstrated increased expression in several immunologic related genes, mitogenic signaling, and epigenetic signaling genes. Using the PANTHER GO-Slim biological process pathway analysis, we identified enrichment of processes involved in biosynthesis, metabolism including oxidative phosphorylation, and Wnt signaling. Using gene set enrichment analysis, we observed enrichment in oxidative phosphorylation, fatty acid metabolism, and glutathione metabolism as well as MYC, P53-dependent DNA damage repair, and NRF2 pathway gene expression among the recurrent HPV-associated OPSCCs.

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Recurrent Human Papillomavirus-Related Head and Neck Cancer Undergoes Metabolic Reprogramming and Is Driven by Oxidative Phosphorylation.

Project description:PurposeHuman papillomavirus (HPV) infection drives the development of some head and neck squamous cell carcinomas (HNSCC). This disease is rapidly increasing in incidence worldwide. Although these tumors are sensitive to treatment, approximately 10% of patients fail therapy. However, the mechanisms that underlie treatment failure remain unclear.Experimental designWe performed RNA sequencing (RNA-seq) on tissues from matched primary- (pHNSCC) and metachronous-recurrent cancers (rHNSCC) to identify transcriptional differences to gain mechanistic insight into the evolutionary adaptations of metachronous-recurrent tumors. We used HPV-related HNSCC cells lines to investigate the effect of (i) NRF2 overexpression on growth in vitro and in vivo, (ii) oxidative phosphorylation (OXPHOS) inhibition using IACS-010759 on NRF2-dependent cells, and (iii) combination of cisplatin and OXPHOS inhibition.ResultsThe OXPHOS pathway is enriched in recurrent HPV-associated HNSCC and may contribute to treatment failure. NRF2-enriched HNSCC samples from The Cancer Genome Atlas (TCGA) with enrichment in OXPHOS, fatty-acid metabolism, Myc, Mtor, reactive oxygen species (ROS), and glycolytic signaling networks exhibited worse survival. HPV-positive HNSCC cells demonstrated sensitivity to the OXPHOS inhibitor, in a NRF2-dependent manner. Further, using murine xenograft models, we identified NRF2 as a driver of tumor growth. Mechanistically, NRF2 drives ROS and mitochondrial respiration, and NRF2 is a critical regulator of redox homeostasis that can be crippled by disruption of OXPHOS. NRF2 also mediated cisplatin sensitivity in endogenously overexpressing primary HPV-related HNSCC cells.ConclusionsThese results unveil a paradigm-shifting translational target harnessing NRF2-mediated metabolic reprogramming in HPV-related HNSCC.

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