Evidence map›Paper›PMID 27293994›Full record

ArticleAmerican journal of cancer research2016

YAP/TAZ regulates the insulin signaling via IRS1/2 in endometrial cancer.

Chao Wang, Kangjin Jeong, Hongyuan Jiang, Wei Guo, Chao Gu, Yiling Lu, Jiyong Liang

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.2field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  14. Targeting Transcription Factors in Cancer: From "Undruggable" to "Druggable".Methods in molecular biology (Clifton, N.J.) · 2023
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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 2 countries.

Chao WangDepartment of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital, Fudan UniversityShanghai 200011, China; Department of Systems Biology, The University of Texas MD Anderson Cancer CenterHouston 77030, TX, USA.
Kangjin JeongDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center Houston 77030, TX, USA.
Hongyuan JiangDepartment of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital, Fudan University Shanghai 200011, China.
Wei GuoDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center Houston 77030, TX, USA.
Chao GuDepartment of Obstetrics and Gynecology, Obstetrics and Gynecology Hospital, Fudan University Shanghai 200011, China.
Yiling LuDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center Houston 77030, TX, USA.
Jiyong LiangDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center Houston 77030, TX, USA.
The University of Texas MD Anderson Cancer Center · USObstetrics and Gynecology Hospital of Fudan University · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Insulin resistance (IR) is an important mechanism of pathogenesis of endometrial cancer (EC) and explains the pathogenic mechanism of high risk factors including Obesity BMI (body mass index), Type 2 Diabetes Mellitus, PCOS and so on. Relieving IR or inhibiting the function of insulin could be one of the potential therapeutic strategies for EC, which is a PI3K-driven disease. PI3K/Akt are the central mediators for insulin/IGF1 signaling, however, the involvement of HIPPO pathway co-activators, YAP and TAZ, in insulin resistance remains to be elucidated. In the present study, we analyzed the clinical and biological data of EC patients from TCGA and observed a correlation between insulin resistance and EC. By comparing the expression level of IRS1/2 in obese vs non-obese patients, we found that the most important insulin resistance relative (IRR) genes are the contributing factors to IR. Interestingly, IRS1/2 was correlated positively with YAP/TAZ in EC patients. Knockdown of YAP/TAZ by specific siRNA inhibited the phosphorylation of IRS1 while increased the phosphorylation of IGFR1, the inhibitor of insulin signaling. Treating EC with siYAP/TAZ, YAP inhibitor Verteporfin or metformin alone only partially inhibited the function of insulin and IGF1. However, combination of siYAP/TAZ with metformin could completely inhibit the effects of insulin. Thus, our study demonstrated a novel function of YAP and TAZ in the insulin resistance via IRS1/2 in endometrial cancer. Our study also provided the rationale for the potential therapeutic treatment of EC with the combination of inhibiting YAP/TAZ and metformin.

Indexed as

endometrial cancerinsulin signalingIRS1/2YAP/TAZ

Identifiers

PMID27293994
PMCPMC4889715
OpenAlexW2462423734

What OpenQuestion holds

Textmetadata
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.