Evidence map›Paper›PMID 38582508›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Phosphorylation of IDH1 Facilitates Progestin Resistance in Endometrial Cancer.

Jingjie Li, Zuoshu Qin, Yunqi Li, Baozhu Huang, Qimeng Xiao, Peiqin Chen, Yifan Luo, Wenxin Zheng, Tao Zhang, Zhenbo Zhang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. CRL4International journal of biological sciences · 2026
    Article
  2. Article
  3. Review
  4. Phosphorylation of IDH1 Facilitates Progestin Resistance in Endometrial Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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

10 authors at 3 institutions in 2 countries.

Jingjie LiPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Zuoshu QinPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yunqi LiShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Baozhu HuangPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Qimeng XiaoPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Peiqin ChenPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yifan LuoPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Wenxin ZhengDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Tao ZhangDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.ORCID 0000-0002-5578-9913
Zhenbo ZhangPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Shanghai Jiao Tong University · CNThe University of Texas Southwestern Medical Center · USTongji University · CN

Funding

Cross- and jointly project 2023-3-ZD-02Fundamental Research Funds for the Central Universities 22120230312National Key Technology R&D Program of China 2019YFC1005200National Key Technology R&D Program of China 2019YFC1005201National Natural Science Foundation of China 82172784National Natural Science Foundation of China 82371642Science and Technology Commission of Shanghai Municipality 23DZ2202100Shanghai Science and Technology Commission 23DZ2202100start funding (RCQD2307) from Shanghai Tongji hospitalTongji University
6 · The paper itself

Abstract

The progestin regimen is one of the main therapeutic strategies for women with endometrial cancer who undergo conservative management. Although many patients respond well to initial therapy, progestin-refractory disease inevitably emerges, and the molecular basis underlying progestin resistance has not been comprehensively elucidated. Herein, they demonstrated progestin results in p38-dependent IDH1 Thr 77 phosphorylation (pT77-IDH1). pT77-IDH1 translocates into the nucleus and is recruited to chromatin through its interaction with OCT6. IDH1-produced α-ketoglutarate (αKG) then facilitates the activity of OCT6 to promote focal adhesion related target gene transcription to confer progestin resistance. Pharmacological inhibition of p38 or focal adhesion signaling sensitizes endometrial cancer cells to progestin in vivo. The study reveals p38-dependent pT77-IDH1 as a key mediator of progestin resistance and a promising target for improving the efficacy of progestin therapy.

Indexed as

Drug Resistance, NeoplasmEndometrial NeoplasmsIsocitrate DehydrogenaseProgestinsAnimalsCell Line, TumorDisease Models, AnimalFemaleHumansMicePhosphorylationIDH1 protein, humanIsocitrate DehydrogenaseProgestinsendometrial cancerIDH1 phosphorylationp38progestin resistance

Identifiers

PMID38582508
PMCPMC11187910
OpenAlexW4394008392

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.