Evidence map›Paper›PMID 40421484›Full record

ArticleEuropean journal of histochemistry : EJH2025

E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway.

Zhijing Wang, Xiaohua Qin, Shanshan Liu, Yilei Wen, Bikan Lan, Hantao Liao, Haixian Wei

Abstract read
In one paragraph

Article in European journal of histochemistry : EJH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

7 authors.

Zhijing WangDepartment of Pathology, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Xiaohua QinDepartment of Pathology, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Shanshan LiuDepartment of Pathology, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Yilei WenDepartment of Pathology, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Bikan LanDepartment of Pathology, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Hantao LiaoSchool of Basic Science, Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.
Haixian WeiSchool of Basic Science, Guangxi University of Traditional Chinese Medicine, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and is involved in the occurrence of various malignant tumor. However, the mechanisms by which E-cadherin regulates tumor metastasis in CRC remain unclear. We established sh-E-cad (silenced by short hairpin RNA) and rescue-E-cad (overexpressed by E-cad plasmid transfection) CRC cell lines to investigate the role of E-cad in CRC in vitro. Immunohistochemistry, clonogenic assays, scratch wound healing assays, CCK-8 assays, flow cytometry, Transwell assay, real time-PCR and Western blot were employed to investigate the underlying mechanisms by which E-cad involve the progression of CRC. In CRC tissues, E-cad expression was significantly reduced, while YAP expression was markedly elevated. Silencing E-cad induced a significant increase of clonogenic ability in CRC cells, which was reduced upon rescue of E-cad expression. Transwell assays indicate that low expression of E-cad enhances the cell migration, a finding corroborated by scratch wound healing experiments. CCK-8 results demonstrate that silencing E-cad promotes the proliferation of CRC cells. Importantly, we found that E-cad influences apoptosis rather than the cell cycle. Analysis of Hippo signaling pathway-related factors revealed that silencing E-cad resulted in significantly decreased expression of MST1/2 and LATS1/2, as well as reduced phosphorylation levels of YAP, while YAP expression was significantly increased. Additionally, immunofluorescence confirmed the nuclear translocation of YAP. Our study indicates that E-cad regulates the malignant progression of CRC via the Hippo signaling pathway, offering a potential new strategy for CRC treatment.

Indexed as

Antigens, CDCadherinsCell MovementCell ProliferationColorectal NeoplasmsProtein Serine-Threonine KinasesSignal TransductionApoptosisCell Line, TumorHippo Signaling PathwayHumansYAP-Signaling ProteinsAntigens, CDCadherinsCDH1 protein, humanProtein Serine-Threonine KinasesYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID40421484
PMCPMC12172619

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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.