Evidence map›Paper›PMID 31057403›Full record

ArticleFrontiers in pharmacology2019

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway.

Lei Liu, Lin Zhang, Shuo Zhao, Xu-Yang Zhao, Peng-Xiang Min, Ya-Dong Ma, Yue-Yuan Wang, Yan Chen, Si-Jie Tang, Yu-Jie Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

35 citing papers in PubMed, 40 citations in OpenAlex.

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  6. How Functional Variants Reconfigure the Rac2 Conformational Landscape.bioRxiv : the preprint server for biology · 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

12 authors at 2 institutions in 1 country.

Lei LiuDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
Lin ZhangDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
Shuo ZhaoDepartment of Physiology, Nanjing Medical University, Nanjing, China.
Xu-Yang ZhaoDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
Peng-Xiang MinDepartment of Physiology, Nanjing Medical University, Nanjing, China.
Ya-Dong MaDepartment of Physiology, Nanjing Medical University, Nanjing, China.
Yue-Yuan WangDepartment of Physiology, Nanjing Medical University, Nanjing, China.
Yan ChenDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
Si-Jie TangDepartment of Physiology, Nanjing Medical University, Nanjing, China.
Yu-Jie ZhangJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Jun DuJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Luo GuJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cell migration is a critical step in cancer metastasis. Over-activated Notch pathway can promote the migration of cancer cells, especially in the breast cancer. However, the underlying mechanism of non-canonical Notch signaling in modulating the migration has not yet been clearly characterized. Here we demonstrated that DAPT, a gamma secretase inhibitor, inhibited protrusion formation and cell motility, and then reduced the migration of triple-negative breast cancer cells, through increasing the activity of Cdc42 by non-canonical Notch pathway. Phosphorylation of AKT on S473 was surprisingly increased when Notch signaling was inhibited by DAPT. Inhibition of PI3K and AKT by LY294002 and MK2206, respectively, or knockdown of AKT expression by siRNA blocked DAPT-induced activation of Cdc42. Moreover, immunofluorescence staining further showed that DAPT treatment reduced the formation of lamellipodia and induced actin cytoskeleton remodeling. Taken together, these results indicated that DAPT inhibited Notch signaling and consequently activated PI3K/AKT/Cdc42 signaling by non-canonical pathway, facilitated the formation of filopodia and inhibited the assembly of lamellipodia, and finally resulted in the decrease of migration activity of breast cancer cells.

Indexed as

actin cytoskeletonCdc42membrane protrusionsnon-canonical NotchPI3K/AKT

Identifiers

PMID31057403
PMCPMC6477508
OpenAlexW2936075892

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.