Evidence map›Paper›PMID 33431816›Full record

ArticleCell death discovery2021

GDF15 promotes glioma stem cell-like phenotype via regulation of ERK1/2-c-Fos-LIF signaling.

Shan Zhu, Ning Yang, Yi Guan, Xue Wang, Guoxia Zang, Xinping Lv, Shuanglin Deng, Wan Wang, Tete Li, Jingtao Chen

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Shan ZhuInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Ning YangInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Yi GuanDepartment of Neurosurgery, The First Hospital of Jilin University, Changchun, China.
Xue WangInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Guoxia ZangInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Xinping LvInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Shuanglin DengDepartment of Neurosurgery, The First Hospital of Jilin University, Changchun, China.
Wan WangInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Tete LiInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jingtao ChenInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China. jtchen@jlu.edu.cn.ORCID http://orcid.org/0000-0002-4720-4225
Jilin University · CN

Funding

Department of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 20180101097JCDepartment of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 20200201503JCDepartment of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 20200201588JCEducation Department of Jilin Province (Jilin Provincial Department Education) JJKH20190043KJJilin University (JLU) 2017TD-08National Natural Science Foundation of China (National Science Foundation of China) 81402436National Natural Science Foundation of China (National Science Foundation of China) 81870152
6 · The paper itself

Abstract

Growth differentiation factor 15 (GDF15), a member of the transforming growth factor β family, is associated with tumor progression, metastasis, and cell apoptosis. However, controversy persists regarding the role of GDF15 in different tumor types, and its function in glioma stem cells (GSCs) remains unknown. Here, we report that GDF15 promotes the GSC-like phenotype in GSC-like cells (GSCLCs) through the activation of leukemia inhibitor factor (LIF)-STAT3 signaling. Mechanistically, GDF15 was found to upregulate expression of the transcription factor c-Fos, which binds to the LIF promoter, leading to enhanced transcription of LIF in GSCLCs. Furthermore, GDF15 may activate the ERK1/2 signaling pathway in GSCLCs, and the upregulation of LIF expression and the GSC-like phenotype was dependent on ERK1/2 signaling. In addition, the small immunomodulator imiquimod induced GDF15 expression, which in turn activated the LIF-STAT3 pathway and subsequently promoted the GSC-like phenotype in GSCLCs. Thus, our results demonstrate that GDF15 can act as a proliferative and pro-stemness factor for GSCs, and therefore, it may represent a potential therapeutic target in glioma treatment.

Identifiers

PMID33431816
PMCPMC7801449
OpenAlexW3118764861

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.