Evidence map›Paper›PMID 24860782›Full record

ReviewFrontiers in oncology2014

Mysteries of TGF-β Paradox in Benign and Malignant Cells.

Qiang Zhang, Nengwang Yu, Chung Lee

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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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

3 authors at 3 institutions in 2 countries.

Qiang ZhangDepartment of Urology, Northwestern University School of Medicine , Chicago, IL , USA.
Nengwang YuDepartment of Urology, General Hospital of Jinan Military Command , Jinan , China.
Chung LeeDepartment of Urology, Northwestern University School of Medicine , Chicago, IL , USA ; Department of Surgery, NorthShore University HealthSystem, Evanston Hospital , Evanston, IL , USA ; Department of Pathology and Laboratory Medicine, University of California at Irvine , Irvine, CA , USA ; Department of Urology, University of California at Irvine , Irvine, CA , USA.
General Hospital of Jinan Military Command · CNNorthShore University HealthSystem · USNorthwestern University · US

Funding

SUPPRESSIVE ROLE OF ANDROGEN RESPONSE GENE CALRETICULIN IN PROSTATE CANCERP50CA090386 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CRAWFORD, SUSAN · 2001 to 2013
$25.1M
Evaluation of Predictive Signatures of Prostate CancerU01CA114810 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI MERCOLA, DAN · 2005 to 2009
$8.2M
The Prostate Cancer Tumor Microenvironment Exhibits Differentially Expressed GeneU01CA152738 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LEE, CHUNG, MERCOLA, DAN · 2010 to 2015
$3.6M
NCI NIH HHS P50 CA090386NCI NIH HHS U01 CA114810NCI NIH HHS U01 CA152738
6 · The paper itself

Abstract

TGF-β regulates a wide range of biological functions including embryonic development, wound healing, organogenesis, immune modulation, and cancer progression. Interestingly, TGF-β is known to inhibit cell growth in benign cells but promote progression in cancer cells; this phenomenon is known as TGF-β paradox. To date, the mechanism of this paradox still remains a scientific mystery. In this review, we present our experience, along with the literature, in an attempt to answer this mystery. First, we observed that, on TGF-β engagement, there is a differential activation of Erk between benign and cancer cells. Since activated Erk is a major mediator in tumor progression and metastasis, a differentially activated Erk represents the answer to this mystery. Second, we identified a key player, PP2A-B56α, which is differentially recruited by the activated type I TGF-β receptor (TBRI) in benign and tumor cells, resulting in differential Erk activation. Finally, TGF-β stimulation leads to suppressed TBRs in tumor cells but not in benign cells. This differentially suppressed TBRs triggers differential recruitment of PP2A-B56α and, thus, differential activation of Erk. The above three events explain the mysteries of TGF-β paradox. Understanding the mechanism of TGF-β paradox will help us to predict indolent from aggressive cancers and develop novel anti-cancer strategies.

Indexed as

Erk activationnegative feedbackpositive feedbackPP2A recruitmentSmad activationTGF-β auto-inductionTGF-β paradoxTGF-β receptors

Identifiers

PMID24860782
PMCPMC4026682
OpenAlexW2005779705

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.