Evidence map›Paper›PMID 33175572›Full record

ReviewAmerican journal of physiology. Cell physiology2021

The mechanobiome: a goldmine for cancer therapeutics.

Eleana Parajón, Alexandra Surcel, Douglas N Robinson

Abstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Ras-mediated dynamic and biphasic regulation of cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024
    Review
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4 · The record

Corrections and comments

  • Commented on by
    2021
5 · Who and what money

Authors and funding

3 authors.

Eleana ParajónDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Alexandra SurcelDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Douglas N RobinsonDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0003-1236-4891

Funding

The Biochemical Basis for the Mechanics of CytokinesisR01GM066817 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ROBINSON, DOUGLAS N · 2003 to 2025
$7.3M
Actin-myosin contractility promotes the development of chronic bronchitisR01HL124099 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SIDHAYE, VENKATARAMANA K · 2017 to 2021
$2.1M
NHLBI NIH HHS R01 HL124099NIGMS NIH HHS R01 GM066817
6 · The paper itself

Abstract

Cancer progression is dependent on heightened mechanical adaptation, both for the cells' ability to change shape and to interact with varying mechanical environments. This type of adaptation is dependent on mechanoresponsive proteins that sense and respond to mechanical stress, as well as their regulators. Mechanoresponsive proteins are part of the mechanobiome, which is the larger network that constitutes the cell's mechanical systems that are also highly integrated with many other cellular systems, such as gene expression, metabolism, and signaling. Despite the altered expression patterns of key mechanobiome proteins across many different cancer types, pharmaceutical targeting of these proteins has been overlooked. Here, we review the biochemistry of key mechanoresponsive proteins, specifically nonmuscle myosin II, α-actinins, and filamins, as well as the partnering proteins 14-3-3 and CLP36. We also examined a wide range of data sets to assess how gene and protein expression levels of these proteins are altered across many different cancer types. Finally, we determined the potential of targeting these proteins to mitigate invasion or metastasis and suggest that the mechanobiome is a goldmine of opportunity for anticancer drug discovery and development.

Indexed as

Actin CytoskeletonActininAnimalsFilaminsGene ExpressionHumansMyosin Type IINeoplasmsSignal TransductionActininFilaminsMyosin Type IIfilaminmechanoresponsemetastasismyosinα-actinin

Identifiers

PMID33175572
PMCPMC8294625

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.