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Label-free Proteomics of Exosomes and Cell Lines from HPV-positive and HPV-negative HNSCC

ABSTRACT: This study investigates the influence of human papillomavirus (HPV) on the proteomic content of exosomes derived from head and neck squamous cell carcinoma (HNSCC) cell lines. Label-free quantitative proteomics was used to analyze exosomes and parental cells from HPV16-positive (93VU147T, UDSCC2) and HPV-negative (OCT-1) HNSCC cell lines. Raw LC-MS/MS data were acquired to study differentially exported proteins, with emphasis on exosomal cargo variation and its functional implications.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Malignant Cell, Cell Culture

DISEASE(S): Head And Neck Squamous Cell Carcinoma

SUBMITTER: Alok Bharti

LAB HEAD: Prof. Alok Chandra Bharti

PROVIDER: PXD067001 | Pride | 2026-07-06

REPOSITORIES: Pride

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			Action	DRS
	CELL_4.raw	Raw
	CELL_4.txt	Txt
	CELL_5.raw	Raw
	CELL_5.txt	Txt
	CELL_6.raw	Raw

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Publications

Proteomic Profiling of Exosomes from HPV-Positive and HPV-Negative Head and Neck Squamous Cell Carcinoma: Selective Cargo Packaging.

Yadav Joni J Tripathi Tanya T Tanwar Neha N Sharma Nupur N Chaudhary Apoorva A Janjua Divya D Joshi Udit U Aggarwal Nikita N Chhokar Arun A Senrung Anna A Maras Jaswinder Singh JS Bharti Alok Chandra AC

Journal of proteome research 20260801 8

Oncogenic viruses, such as human papillomavirus (HPV), alter the endosomal system to manipulate the proteomic content of extracellular vesicles, aiding their persistence and disease progression. HPV has emerged as a key risk factor for head and neck squamous cell carcinoma (HNSCC). However, the influence of HPV on the exosomal proteomics remains poorly understood. Label-free quantitative proteomics was employed to analyze proteins extracted from HPV16-positive (93VU147T, UDSCC2) and HPV-negative ...[more]

PMID: 42372200

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Comparison between HPV+ / p16+ versus the HPV-/p16- from HNSCC patients

Project description:Head and neck squamous cell carcinomas are heterogeneous neoplasms that show clinical and biological differences in association with the human papillomavirus (HPV). To provide adequate therapeutic strategies, biological and clinical characterization is essential to stratify patients based on prognostic and predictive factors. Reports on HNSCC are scarce in Mexico, thus in the present study, we analyze 414 cases of HNSCC, including those of the oropharynx (OPSCC), larynx (LASCC), and oral cavity (OCSCC). We determined the presence of HPV and p16 expression. Global expression profiles were analyzed with Affymetrix HTA 2.0 microarray in 25 selected cases HPV+/p16+ versus HPV-/p16-. In our study we analyze 25 samples derived from HNSCC patients. 18 samples were HPV-/p16- and 7 HPV+/p16+. We compared the HPV-/p16- versus the HPV+/p16+ and identified differentially expressed RNAs with a fold change greater than 1.5 or less than -1.5. These data were used to obtain 98 genes that are differentially expressed in absence of HPV. The present study offers information regarding clinical and molecular characteristics of HNSCC, both associated and unassociated with HPV, in Mexican patients.

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Methylome Analysis of FF HPV+ and HPV- HNSCC samples

Project description:The analysis of the 6 methylomes by MeDIP-Seq comprise 3 HPV+ HNSCC samples and 3 HPV- HNSCC samples Analysis of the 6 methylomes, comprising 3 HPV+ HNSCC samples and 3 HPV- HNSCC samples

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450k Analysis of 42 FFPE HPV+ and HPV- HNSCC samples

Project description:The methylation analysis of 21 FFPE HPV+ HNSCC samples and 21 FPPE HPV- HNSCC samples by Infinium HumanMethylation450 BeadChip Analysis of 42 450k methylation profiles, comprising 21 HPV+ HNSCC samples and 21 HPV- HNSCC samples

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Copy Number Alterations in HNSCC with or without Oncogene Expressing Human Papillomavirus

Project description:Oncogene expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, reflected by a low level of mutations in TP53 and allelic loss at 3p, 9p and 17p, genetic changes frequently found in HNSCCs of non-viral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and one by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high resolution micro-array comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, 20p-20q and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression.

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NSD2 is upregulated by high-risk HPV E6/E7 and modulates epithelial differentiation in HPV-associated Head and Neck Cancer

Project description:Epigenetic alterations are a key hallmark of cancer and are increasingly recognized as promising clinical biomarkers and therapeutic targets. Head and Neck Squamous Cell Carcinomas (HNSCC) are classified into two subtypes: HPV-positive (HPV+), driven by human papillomavirus (HPV) infections, and the HPV-negative (HPV-), associated with environmental risk factors. Although exhibiting distinct molecular and clinicopathological features, both subtypes lack effective, tailored therapies. Profiling their epigenetic landscape could thus have important clinical implications. In this study, we employed a quantitative mass spectrometry approach to profile histone post-translational modification (hPTMs) in HPV+ and HPV- HNSCC.

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