Evidence map›Paper›PMID 32728066›Full record

ArticleScientific reports2020

PTEN suppresses epithelial-mesenchymal transition and cancer stem cell activity by downregulating Abi1.

Yanmei Qi, Jie Liu, Joshua Chao, Mark P Scheuerman, Saum A Rahimi, Leonard Y Lee, Shaohua Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. PI3 K/AKT/mTOR pathway and its role in breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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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

7 authors at 2 institutions in 1 country.

Yanmei QiDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Jie LiuDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Joshua ChaoDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Mark P ScheuermanDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Saum A RahimiDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Leonard Y LeeDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Shaohua LiDepartment of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA. shaohua.li@rutgers.edu.
Johnson University · USRutgers, The State University of New Jersey · US

Funding

Regulation of epithelial-mesenchymal transition and stem cell activity by PTEN in breast cancerR21CA201715 · NCI · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI LI, SHAOHUA · 2016 to 2017
$363k
NCI NIH HHS R21 CA201715NCI NIH HHS R21CA201715
6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is an embryonic program frequently reactivated during cancer progression and is implicated in cancer invasion and metastasis. Cancer cells can also acquire stem cell properties to self-renew and give rise to new tumors through the EMT. Inactivation of the tumor suppressor PTEN has been shown to induce the EMT, but the underlying molecular mechanisms are less understood. In this study, we reconstituted PTEN-deficient breast cancer cells with wild-type and mutant PTEN, demonstrating that restoration of PTEN expression converted cancer cells with mesenchymal traits to an epithelial phenotype and inhibited cancer stem cell (CSC) activity. The protein rather than the lipid phosphatase activity of PTEN accounts for the reversal of the EMT. PTEN dephosphorylates and downregulates Abi1 in breast cancer cells. Gain- and loss-of-function analysis indicates that upregulation of Abi1 mediates PTEN loss-induced EMT and CSC activity. These results suggest that PTEN may suppress breast cancer invasion and metastasis via dephosphorylating and downregulating Abi1.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCell Line, TumorCell MovementCytoskeletal ProteinsDown-RegulationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMiceMice, KnockoutNeoplastic Stem CellsPhosphorylationABI1 protein, humanAdaptor Proteins, Signal TransducingCytoskeletal ProteinsPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID32728066
PMCPMC7391766
OpenAlexW3045810123

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.