Dataset Information

Data-independent acquisition proteomics enhances cellular nucleic acid binding protein characterization in colitis data3

ABSTRACT: We developed a robust workflow for in-depth analysis of NABPs, which combining immobilized metal affinity chromatography capture and data-independent acquisition. This workflow enhances the identification and quantification of NABPs. We then applied this workflow to colitis mouse and discovered epigenetic processes, particularly histone methylation was significantly changed in spleen.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spleen

SUBMITTER: Huiyu Wang

LAB HEAD: Hua Xiao

PROVIDER: PXD054787 | Pride | 2025-12-01

REPOSITORIES: Pride

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Publications

Massive deciphering of the tissue nucleic acid-binding proteome via affinity chromatography integrated with data-independent acquisition-based proteomics.

Wang Huiyu H Zhu Jianzheng J Li Suntao S Zhang Lu L Guo Miao M Zhao Jiaqi J Zhang Yan Y Cao Chengxi C Hu Shen S Xiao Hua H

Nucleic acids research 20251101 21

The development of inflammatory bowel disease is driven by transcriptional and epigenetic regulators of the nucleic acid-binding proteome (NABPome). However, comprehensive analysis of NABPome composition and dynamics remains challenging due to the lack of an in-depth proteomics strategy. Here, we developed an NABP-DIA methodology that integrates NABPome capture with data-independent acquisition (DIA)-based proteomics. Using NABP-DIA with an experimentally generated spectral library, we achieved ...[more]

PMID: 41261858

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Project description:The global rise of HPV(+) oropharyngeal squamous cell carcinoma (OPSCC) has generated considerable interest underlying its etiology and management. Despite an overall decline in head and neck malignancies, the incidence in OPSCC has by contrast sharply risen, with HPV(+) subtypes now comprising 80% of all OPSCC.1,2 Relative to HPV(-) OPSCC, HPV(+) patients are more responsive to chemoradiation and harbor a 52% risk-of-death reduction.3 Despite this distinct outcome, treatment regimens remain the same for all OPSCC subtypes (smoking-driven and virus-driven), rather than an adaptive approach to what most consider distinct diseases. The short-term effects (e.g., mucositis, odynophagia) and long-term toxicities (e.g., xerostomia, dysphagia, ototoxicity) from treatment substantially affect quality of life, and rival the impact of the cancer itself. Recently published as well as ongoing trials are actively examining deintensification approaches2,4-9, with the goal of diminishing treatment sequelae for HPV(+) subtypes. While deintensification may decrease chemoradiation-related toxicities, it nonetheless may also undertreat a meaningful percentage of HPV(+) patients who may then recur. In examining national trials, 19% of HPV(+) patients had disease progression after therapy, with a two-year survival rate of 60%.10 Current methods to ascertain HPV status involve p16 staining. However, on comparison with gold standard E6/E7 expression by qPCR, p16 harbored a 15% false positivity rate11, suggesting limited utility as a sole biomarker for deintensification. Improved molecular stratification would greatly enhance the clinician’s ability to precisely tailor treatment while minimizing the risk of jeopardizing outcomes. One approach encompasses in-depth proteomic profiling of HPV(+) OPSCC to reveal distinct protein expression profiles and delineate clinically relevant upstream pathways. In turn, these proteomic differences may distinguish higher-risk disease (cases predisposed to recurrence that may benefit from treatment intensification) from lower-risk phenotypes (cases whose treatment response is sufficiently robust to warrant deintensification). Here, two HPV(+) OPSCC cohorts stratified by treatment response are compared via a hybrid data dependent acquisition/data independent acquisition (DDA/DIA) approach via mass spectrometry. We focused on detection of low-abundance proteins to highlight proteomic signatures that can be potentially exploited for treatment stratification.

			Action	DRS
	spleen_report.pg_matrix.tsv	Tabular
	spleennabpWCC1.wiff	Wiff
	spleennabpWCC1.wiff.scan	Wiff
	spleennabpWCC2.wiff	Wiff
	spleennabpWCC2.wiff.scan	Wiff