ArticleACS chemical biology2020
A Proteomic Connectivity Map for Characterizing the Tumor Adaptive Response to Small Molecule Chemical Perturbagens.
Article in ACS chemical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Development and verification of a comprehensive diagnostic model for osteosarcoma using random forest and artificial neural network.Discover oncology · 2026Article
- An expanded role for single-cell chemical genomics profiling in drug discovery.The Biochemical journal · 2026Review
- Proteomic-based stemness score measures oncogenic dedifferentiation and enables the identification of druggable targets.Cell genomics · 2025Article
- Extreme-Phenotype Genome-Wide Association Analysis for Growth Traits in Spotted Sea Bass (Animals : an open access journal from MDPI · 2024Article
- Structural and Biochemical Insights into Post-Translational Arginine-to-Ornithine Peptide Modifications by an Atypical Arginase.ACS chemical biology · 2023Article
- Quantitative phosphoproteomic analyses identify STK11IP as a lysosome-specific substrate of mTORC1 that regulates lysosomal acidification.Nature communications · 2022Article
- Early Diagnosis and Screening for Lung Cancer.Cold Spring Harbor perspectives in medicine · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
A powerful means to understand the cellular function of corrupt oncogenic signaling programs requires perturbing the system and monitoring the downstream consequences. Here, using a unique pair of non-small cell lung cancer (NSCLC)/normal lung epithelial patient-derived cell lines (HCC4017/HBEC30KT), we systematically interrogated the remodeling of the NSCLC proteome upon treatment with 35 chemical perturbagens targeting a diverse array of mechanistic classes. HCC4017 and HBEC30KT cells differ significantly in their proteomic response to the same compound treatment. Using protein covariance analyses, we identified a large number of functional protein networks. For example, we found that a poorly studied protein, C5orf22, is a novel component of the WBP11/PQBP1 splicing complex. Depletion of C5orf22 leads to the aberrant splicing and expression of genes involved in cell growth and immunomodulation. In summary, we show that by systematically measuring the tumor adaptive responses at the proteomic level, an understanding could be generated that provides critical circuit-level biological insights for these pharmacologic perturbagens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.