Evidence map›Paper›PMID 38310132›Full record

ArticleScientific reports2024

Mechanical activation and expression of HSP27 in epithelial ovarian cancer.

Molly Buckley, Maranda Kramer, Bronte Johnson, Gillian Huskin, Joel Berry, Mary Kathryn Sewell-Loftin

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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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

6 authors at 1 institution in 1 country.

Molly Buckley *Department of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK.
Maranda Kramer *Department of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK.
Bronte JohnsonDepartment of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK.
Gillian HuskinDepartment of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK.
Joel BerryDepartment of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK.
Mary Kathryn Sewell-LoftinDepartment of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, UK. mksewellloftin@uab.edu.ORCID 0000-0003-1985-6899
University of Alabama at Birmingham · US

Funding

Development and Functional Assessment of Cardiovascular Tissue Engineering Therapy (CVTE) T32 Training GrantT32EB023872 · NIBIB · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROGERS, JACK M, ZHANG, JIANYI · 2018 to 2022
$753k
Biomechanical Regulation of Angiogenesis during Tumor ProgressionR00CA230202 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SEWELL-LOFTIN, MARY KATHRYN · 2020 to 2022
$705k
Biomechanical Regulation of Angiogenesis during Tumor ProgressionK99CA230202 · NCI · WASHINGTON UNIVERSITY · PI SEWELL-LOFTIN, MARY KATHRYN · 2018 to 2019
$182k
NCI NIH HHS CA230202NCI NIH HHS K99 CA230202NCI NIH HHS R00 CA230202NHLBI NIH HHS EB023872NIBIB NIH HHS T32 EB023872
6 · The paper itself

Abstract

Understanding the complex biomechanical tumor microenvironment (TME) is of critical importance in developing the next generation of anti-cancer treatment strategies. This is especially true in epithelial ovarian cancer (EOC), the deadliest of the gynecologic cancers due to recurrent disease or chemoresistance. However, current models of EOC progression provide little control or ability to monitor how changes in biomechanical parameters alter EOC cell behaviors. In this study, we present a microfluidic device designed to permit biomechanical investigations of the ovarian TME. Using this microtissue system, we describe how biomechanical stimulation in the form of tensile strains upregulate phosphorylation of HSP27, a heat shock protein implicated in ovarian cancer chemoresistance. Furthermore, EOC cells treated with strain demonstrate decreased response to paclitaxel in the in vitro vascularized TME model. The results provide a direct link to biomechanical regulation of HSP27 as a mediator of EOC chemoresistance, possibly explaining the failure of such therapies in some patients. The work presented here lays a foundation to elucidating mechanobiological regulation of EOC progression, including chemoresistance and could provide novel targets for anti-cancer therapeutics.

Indexed as

Neoplasms, Glandular and EpithelialOvarian NeoplasmsCarcinoma, Ovarian EpithelialCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHumansMolecular ChaperonesPaclitaxelTumor MicroenvironmentHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanMolecular ChaperonesPaclitaxel

Identifiers

PMID38310132
PMCPMC10838328
OpenAlexW4391507331

What OpenQuestion holds

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Registered trials

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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.