Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 608

The DOI matches its Crossref record; 85 of the 85 references it cites were found in a registry or an index.

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

Open access
Xu, Wenting, Yang, Zhen, Lu, Nonghua·2015·Cell Adhesion & Migration

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1080/19336918.2015.1016686

Cites

85 of 85 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

1 retracted

Show all 85 references

Cited by

See all 608

Metadata

Authors
Xu, W., Yang, Z., & Lu, N.
Venue
Cell Adhesion & Migration
Published
2015-07-04
Volume
9
Issue
4
Pages
317-324
ISSN
  • 1933-6918 (ISSN-L)
  • 1933-6926
OpenAlex
W1849856438
Cited by
608
References
85
FWCI
9.88
Type
journal article
Language
en
Open access
gold

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition. https://app.cochat.ai/papers/10.1080/19336918.2015.1016686
The paper
Xu, W., Yang, Z., & Lu, N. (2015). A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition. Cell Adhesion & Migration. https://doi.org/10.1080/19336918.2015.1016686

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.