Evidence map›Paper›PMID 26241004›Full record

ReviewCell adhesion & migration2015

A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition.

Wenting Xu, Zhen Yang, Nonghua Lu

Abstract readReview
In one paragraph

Review in Cell adhesion & migration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 371 papers.

0numbers the graph read from it
0cells of the map it votes in
371citing 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

371 citing papers in PubMed.

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311 more citing papers are in PubMed but not listed here.

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

3 authors.

Wenting Xua Department of Gastroenterology ; The First Affiliated Hospital of Nanchang University ; Nanchang , Jiangxi , China.
Zhen Yang
Nonghua Lu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor metastasis is not only a sign of disease severity but also a major factor causing treatment failure and cancer-related death. Therefore, studies on the molecular mechanisms of tumor metastasis are critical for the development of treatments and for the improvement of survival. The epithelial-mesenchymal transition (EMT) is an orderly, polygenic biological process that plays an important role in tumor cell invasion, metastasis and chemoresistance. The complex, multi-step process of EMT involves multiple regulatory mechanisms. Specifically, the PI3K/Akt signaling pathway can affect the EMT in a variety of ways to influence tumor aggressiveness. A better understanding of the regulatory mechanisms related to the EMT can provide a theoretical basis for the early prediction of tumor progression as well as targeted therapy.

Indexed as

AnimalsEpithelial-Mesenchymal TransitionHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktanti-cancer therapybHLH, basic helix-loop-helix proteinCK, cytokeratinECM, extracellular matrixEMTEMT, epithelial-mesenchymal transitionextracellular matrixFGF, fibroblast growth factorGSK-3β, glycogen synthase kinase 3 βILK, integrin-linked kinaseMDR, multidrug resistanceMET, mesenchymal-epithelial transitionPDGF, platelet-derived growth factorPDK1, 3-phosphoinositide-dependent protein kinase 1PI3K/Akt signaling pathwayPI3K, phosphatidylinositol-3-kinasePKA, protein kinase APKB, protein kinase BPKC, protein kinase CTGF-β, transforming growth factor-βTNF-α, tumor necrosis factor-αtranscription factorstumor aggressivenessYB-1, Y-box binding protein-1

Identifiers

PMID26241004
PMCPMC4594353

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.