Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (557 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The movement of cells from one location to another. Distinguish from cytokinesis which is the process of dividing the cytoplasm of a cell.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Cell Movements; Movements, Cell; Movement, Cell; Migration, Cell; Cell Migration; Locomotion, Cell; Cell Locomotion; Motility, Cell.
Where it fits in the MeSH classification
- Broader topics
- Cell Physiological Phenomena; Locomotion
- Narrower topics
- Cell Aggregation; Cell Migration Inhibition; Chemotaxis; Ovum Transport; Sperm Motility; Sperm Transport; Transcellular Cell Migration; Transendothelial and Transepithelial Migration
- See also
- Cell Tracking
Related concepts
- Cytokinesis
- Cytoplasm
Research landscape
PubMed indexes 227,609 records tagged with the MeSH heading “Cell Movement” (counts retrieved 2026-10-29). 50,537 of them (22.2%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 82,126 records.
Reviews account for 17,475 records (7.7%) and meta-analyses for 224. Randomized controlled trials number 658 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 49,772 |
| 2000-2009 | 45,174 |
| 2010-2019 | 82,126 |
| 2020 onward | 50,537 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 17,475 | 7.7% |
| Meta-analyses | 224 | 0.1% |
| Randomized controlled trials | 658 | 0.3% |
Method: PubMed query "Cell Movement"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Clonal-aggregative multicellularity tuned by salinity in a choanoflagellate | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41741645 · DOI · PMC13017551 |
| Long-range mutual activation establishes Rho and Rac polarity during cell migration | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42270977 · DOI · PMC13279283 |
| Cyclin D1/D2-CDK4 Drives Cell Migration by Orchestrating Cytoskeletal Dynamics Through a TGFβ-FAK-Rac1 Axis | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41683655 · DOI · PMC12897814 |
Clonal-aggregative multicellularity tuned by salinity in a choanoflagellate [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Multicellularity evolved independently multiple times in eukaryotes1-4.
- Closing excerpt
- Our findings challenge former generalizations about choanoflagellates and expand the option space of choanozoan multicellularity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
Multicellularity evolved independently multiple times in eukaryotes1-4. Two distinct mechanisms underpin multicellularity5: clonality (serial cell division without sister-cell separation) and aggregation (whereby independent cells assemble into a multicellular entity). Clonal and aggregative multicellularity are traditionally considered to be mutually exclusive1,6-8, with rare exceptions9, and evolutionary hypotheses have addressed why multicellularity might diverge towards one or the other extreme3,4. Both animals and their sister group, the choanoflagellates, are currently known to acquire multicellularity only clonally4,10,11. Here we show that the choanoflagellate Choanoeca flexa12 forms motile and contractile cell monolayers (sheets) through multiple mechanisms-C. flexa sheets can form purely clonally, purely aggregatively or through a combination of both processes. We characterize the life history of C. flexa in its natural environment-ephemeral splash pools on the island of Curaçao-and show that C. flexa undergoes reversible transitions between unicellularity and multicellularity during evaporation-refilling cycles. Different splash pools house genetically distinct strains of C. flexa and kin recognition constrains aggregation between them. We show that clonal-aggregative multicellularity is a versatile strategy for the robust establishment of multicellularity in this variable and fast-fluctuating environment. Our findings challenge former generalizations about choanoflagellates and expand the option space of choanozoan multicellularity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41741645 · DOI · PMC13017551
Long-range mutual activation establishes Rho and Rac polarity during cell migration [2]
Abstract reading summary — source excerpts
- Opening excerpt
- In migrating cells, the GTPase Rac organizes a protrusive front, whereas Rho organizes a contractile back.
- Closing excerpt
- This circuit is required for efficient polarity and migration in primary human T cells and is conserved in epithelial cells, highlighting the generality of this mechanism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)
In migrating cells, the GTPase Rac organizes a protrusive front, whereas Rho organizes a contractile back. How these GTPases are positioned at opposite poles remains unclear. We leverage optogenetics, mechanical perturbations, and mathematical modelling to reveal a surprising mechanochemical long-range mutual activation between front and back polarity programmes that complements their well-known local mutual inhibition. Rac-based protrusions elevate membrane tension, stimulating an mTORC2-dependent activation of Rho at the opposite side of the cell. Conversely, Rho-mediated contractility induces cortical-flow-based regulation of phosphoinositide signalling that triggers Rac activation distally. We develop a minimal mechanochemical model to explain how long-range facilitation, together with local inhibition, enables robust Rho and Rac partitioning. Our findings demonstrate how the actin cortex and plasma membrane interact as an integrated mechanochemical system for long-range Rac-Rho patterning. This circuit is required for efficient polarity and migration in primary human T cells and is conserved in epithelial cells, highlighting the generality of this mechanism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42270977 · DOI · PMC13279283
Cyclin D1/D2-CDK4 Drives Cell Migration by Orchestrating Cytoskeletal Dynamics Through a TGFβ-FAK-Rac1 Axis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Beyond their canonical role in promoting G1/S progression, the complexes formed by cyclin D and cyclin-dependent kinase (CDK) 4/6 have emerged as contributors to enhanced cell migration.
- Closing excerpt
- These findings provide direct evidence that CDK4 regulates actin cytoskeletal reorganization during cell migration and suggest that CDK4/6 inhibitors may dampen cytoskeleton-dependent tumor invasion, in addition to their antiproliferative effects.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (210 words)
Beyond their canonical role in promoting G1/S progression, the complexes formed by cyclin D and cyclin-dependent kinase (CDK) 4/6 have emerged as contributors to enhanced cell migration. However, a direct link between this complex and cytoskeletal remodeling during cell motility has remained poorly understood. Here, we show that CDK4/6 inhibition in HeLa cells disrupts lamellipodia formation and subsequent focal adhesion assembly, leading to a reduction in cell migration and invasion. Notably, CDK4, but not CDK6, in complex with cyclin D1/D2, localizes to membrane ruffles to facilitate cytoskeletal reorganization. Mechanistically, proteomic and phosphoproteomic analyses revealed that CDK4 inhibition attenuates the transforming growth factor β (TGFβ) pathway via reduced Smad3 phosphorylation at Thr8, downregulating integrin subunits (α5, α6, and β1). Furthermore, CDK4 inhibition significantly decreased focal adhesion kinase (FAK) phosphorylation at Tyr397 and Rac1-GTP levels. Importantly, the resulting migration defect was largely restored by activation of either Rac1 or FAK. Thus, our data support a model in which cyclin D1/D2-CDK4 promotes phosphorylation of Smad3, leading to upregulation of integrin subunits, activation of FAK and Rac1, and consequent lamellipodia formation and cell migration. These findings provide direct evidence that CDK4 regulates actin cytoskeletal reorganization during cell migration and suggest that CDK4/6 inhibitors may dampen cytoskeleton-dependent tumor invasion, in addition to their antiproliferative effects.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41683655 · DOI · PMC12897814
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The principles of directed cell migration [4]
- Research article Dendritic cell migration in inflammation and immunity [5]
- Research article EMT, cancer stem cells and autophagy; The three main axes of metastasis [6]
- Research article Cytoskeletal Crosstalk in Cell Migration [7]
- Research article Mechanoresponsive metabolism in cancer cell migration and metastasis [8]
- Research article Multiple functions of flagellar motility and chemotaxis in bacterial physiology [9]
References
- Ros-Rocher N, Reyes-Rivera J, Horo U, Combredet C, Foroughijabbari Y, Larson BT, et al.. Clonal-aggregative multicellularity tuned by salinity in a choanoflagellate. . 2026. PMID 41741645 · DOI · PMC13017551
- De Belly H, Gallén AF, Strickland E, Estrada DC, Godinez DS, Neiva E, et al.. Long-range mutual activation establishes Rho and Rac polarity during cell migration. . 2026. PMID 42270977 · DOI · PMC13279283
- Guo R, Wang Y, Zhang A, Jirawatnotai S, Chu C, Liu L. Cyclin D1/D2-CDK4 Drives Cell Migration by Orchestrating Cytoskeletal Dynamics Through a TGFβ-FAK-Rac1 Axis. . 2026. PMID 41683655 · DOI · PMC12897814
- SenGupta S, Parent CA, Bear JE. The principles of directed cell migration. Nat Rev Mol Cell Biol. 2021. PMID 33990789 · DOI · PMC8663916
- Liu J, Zhang X, Cheng Y, Cao X. Dendritic cell migration in inflammation and immunity. Cell Mol Immunol. 2021. PMID 34302064 · DOI · PMC8298985
- Babaei G, Aziz SG, Jaghi NZZ. EMT, cancer stem cells and autophagy; The three main axes of metastasis. Biomed Pharmacother. 2021. PMID 33227701 · DOI
- Seetharaman S, Etienne-Manneville S. Cytoskeletal Crosstalk in Cell Migration. Trends Cell Biol. 2020. PMID 32674938 · DOI
- Zanotelli MR, Zhang J, Reinhart-King CA. Mechanoresponsive metabolism in cancer cell migration and metastasis. Cell Metab. 2021. PMID 33915111 · DOI · PMC9015673
- Colin R, Ni B, Laganenka L, Sourjik V. Multiple functions of flagellar motility and chemotaxis in bacterial physiology. FEMS Microbiol Rev. 2021. PMID 34227665 · DOI · PMC8632791
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.