Evidence map›Paper›PMID 25100860›Full record

ArticleMolecular & cellular proteomics : MCP2014

Quantitative profiling of chromatome dynamics reveals a novel role for HP1BP3 in hypoxia-induced oncogenesis.

Bamaprasad Dutta, Ren Yan, Sai Kiang Lim, James P Tam, Siu Kwan Sze

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  12. Gene transcription and chromatin regulation in hypoxia.Biochemical Society transactions · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Bamaprasad DuttaFrom the ‡School of Biological Sciences, Nanyang Technological University, 60 Nanyang Dr., Singapore 637551;
Ren YanFrom the ‡School of Biological Sciences, Nanyang Technological University, 60 Nanyang Dr., Singapore 637551;
Sai Kiang Lim§Institute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos, Singapore 138648.
James P TamFrom the ‡School of Biological Sciences, Nanyang Technological University, 60 Nanyang Dr., Singapore 637551;
Siu Kwan SzeFrom the ‡School of Biological Sciences, Nanyang Technological University, 60 Nanyang Dr., Singapore 637551; sksze@ntu.edu.sg.
Nanyang Technological University · SGAgency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast to the intensely studied genetic and epigenetic changes that induce host cell transformation to initiate tumor development, those that promote the malignant progression of cancer remain poorly defined. As emerging evidence suggests that the hypoxic tumor microenvironment could re-model the chromatin-associated proteome (chromatome) to induce epigenetic changes and alter gene expression in cancer cells, we hypothesized that hypoxia-driven evolution of the chromatome promotes malignant changes and the development of therapy resistance in tumor cells. To test this hypothesis, we isolated chromatins from tumor cells treated with varying conditions of normoxia, hypoxia, and re-oxygenation and then partially digested them with DNase I and analyzed them for changes in euchromatin- and heterochromatin-associated proteins using an iTRAQ-based quantitative proteomic approach. We identified a total of 1446 proteins with a high level of confidence, including 819 proteins that were observed to change their chromatin association topology under hypoxic conditions. These hypoxia-sensitive proteins included key mediators of chromatin organization, transcriptional regulation, and DNA repair. Furthermore, our proteomic and functional experiments revealed a novel role for the chromatin organizer protein HP1BP3 in mediating chromatin condensation during hypoxia, leading to increased tumor cell viability, radio-resistance, chemo-resistance, and self-renewal. Taken together, our findings indicate that HP1BP3 is a key mediator of tumor progression and cancer cell acquisition of therapy-resistant traits, and thus might represent a novel therapeutic target in a range of human malignancies.

Indexed as

AnimalsAntineoplastic AgentsCarcinogenesisCarcinoma, Squamous CellCell Line, TumorChromatinDeoxyribonuclease IDNA-Binding ProteinsDoxorubicinDrug Resistance, NeoplasmEpigenesis, GeneticGamma RaysGene Expression ProfilingGene Expression Regulation, NeoplasticHumansHypoxiaAntineoplastic AgentsChromatinDeoxyribonuclease IDNA-Binding ProteinsDoxorubicinHP1BP3 protein, humanNuclear ProteinsProteome

Identifiers

PMID25100860
PMCPMC4256480
OpenAlexW2124182130

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.