Evidence map›Paper›PMID 39671185›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

pERK transition-induced directional mode switching promotes epithelial tumor cell migration.

Huijing Yu, Guanli Xiao, Mingyao Gu, Liting Zhang, Ming Xia, Shimin Mo, Yuying Zhao, Chaoliang Wei

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. ERK builds a population of short-lived nascent adhesions that produce persistent edge protrusion and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

8 authors.

Huijing Yu *Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0009-0004-8521-3941
Guanli Xiao *Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0009-0007-7815-9440
Mingyao Gu *Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0000-0003-1566-753X
Liting ZhangShenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.
Ming XiaShenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0000-0002-4811-7609
Shimin MoShenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0009-0007-5346-3008
Yuying ZhaoShenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.ORCID 0000-0003-4859-834X
Chaoliang WeiShenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.

Funding

National Natural Science Funds of the People's Republic of China 31970729Shenzhen Science and technology innovation committee project JCYJ20180507182239272Shenzhen Science and Technology Program KQTD20190929172538530
6 · The paper itself

Abstract

Increasing evidence suggests that tumor cells exhibit extreme plasticity in migration modes in order to adapt to microenvironments. However, the underlying mechanism for governing the migration mode switching is still unclear. Here, we revealed that epithelial tumor cells could develop a stable directional mode driven by hyperactivated ERK activity. This highly activated and dynamically changing ERK activity, called pERK transition, is crucial for inducing the switch from pauses state to directional movement and is also necessary for maintaining epithelial tumor cells in the directional mode. PERK transition integrated pERK surf, the dynamic and localized ERK activity at the leading edge. The sequential activation of RhoA and Rac1 by pERK transition played critical roles in generation of pERK surf activity through a movement feedback mechanism. PERK transition activity converted the orderly collective migration into the disordered dispersal movement, enhanced the invasiveness of epithelial tumor cells, and promoted their metastasis in immune-deficient mice. These findings revealed that the exquisite spatiotemporal organization of ERK activity orchestrates migration and invasion of tumor cells and provide evidence for the mechanism underlying migration mode switching in epithelial tumor cells.

Indexed as

Cell Movementrac1 GTP-Binding ProteinAnimalsCell Line, TumorEpithelial CellsExtracellular Signal-Regulated MAP KinasesHumansMAP Kinase Signaling SystemMiceNeoplasm InvasivenessrhoA GTP-Binding ProteinExtracellular Signal-Regulated MAP Kinasesrac1 GTP-Binding ProteinRAC1 protein, humanrhoA GTP-Binding Proteinmigration mode switchingmigration plasticitypERK surfpERK transitionrampage mode

Identifiers

PMID39671185
PMCPMC11665884

What OpenQuestion holds

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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.