Evidence map›Paper›PMID 38383297›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

G protein-coupled estrogen receptor activates PI3K/AKT/mTOR signaling to suppress ferroptosis via SREBP1/SCD1-mediated lipogenesis.

Jiaping Chen, Rong Zhao, Yangwei Wang, Han Xiao, Wei Lin, Mingxin Diao, Shiwen He, Peiyuan Mei, Yongde Liao

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
17.6field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 42 citations in OpenAlex.

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  15. Overexpression of GPER1 suppressed esophageal carcinoma growthEuropean journal of histochemistry : EJH · 2026
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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

9 authors at 2 institutions in 1 country.

Jiaping Chen *Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Rong Zhao *Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Yangwei Wang *Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Han XiaoDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Wei LinDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Mingxin DiaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Shiwen HeDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Peiyuan MeiDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. m13260630812@163.com.ORCID 0000-0003-1643-0913
Yongde LiaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. liaoyongde@hust.edu.cn.
Union Hospital · CNShandong Provincial Hospital · CN

Funding

Department of Science and Technology of Hubei Province 2020BCB027National Natural Science Foundation of China No. 82072593
6 · The paper itself

Abstract

backgroundLung cancer is the leading cause of cancer-related death worldwide. The sex differences in the occurrence and fatality rates of non-small cell lung cancer (NSCLC), along with its association with estrogen dependence, suggest that estrogen receptors (ERs) contribute to the development of NSCLC. However, the influence of G protein-coupled estrogen receptor (GPER1) on NSCLC remains to be determined. Escape from ferroptosis is one of the hallmarks of tumor discovered in recent years. In this context, the present study evaluated whether GPER1 promotes NSCLC progression by preventing ferroptosis, and the underlying mechanism through which GPER1 protects against ferroptosis was also explored.

methodsThe effects of GPER1 on the cytotoxicity of H

resultsGPER1 and G1 alleviated the cytotoxicity of H

conclusionGPER1 prevents ferroptosis in NSCLC by promoting the activation of PI3K/AKT/mTOR signaling, thereby inducing SCD1 expression. Therefore, treatments targeting GPER1 combined with cisplatin would exhibit better antitumor effects.

Indexed as

Carcinoma, Non-Small-Cell LungFerroptosisLung NeoplasmsCisplatinEstrogensFemaleGTP-Binding ProteinsHumansHydrogen PeroxideLipogenesisMalePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, G-Protein-CoupledStearoyl-CoA DesaturaseCisplatinEstrogensGTP-Binding ProteinsHydrogen PeroxidePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, G-Protein-CoupledSCD1 protein, humanStearoyl-CoA DesaturaseTOR Serine-Threonine KinasesCisplatin and SCD1FerroptosisGPER1NSCLC

Identifiers

PMID38383297
PMCPMC10880371
OpenAlexW4391996801

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.