Evidence map›Paper›PMID 33753729›Full record

ArticleCell death & disease2021

FGF21 facilitates autophagy in prostate cancer cells by inhibiting the PI3K-Akt-mTOR signaling pathway.

Han Dai, Wenjing Hu, Lianying Zhang, Feiyu Jiang, Xiongmin Mao, Gangyi Yang, Ling Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.8field-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

40 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  7. Review
  8. RUNX1T1 drives stem-like small-cell neuroendocrine prostate cancer identity.Frontiers in cell and developmental biology · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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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 1 country.

Han Dai *The Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Wenjing Hu *Chongqing Prevention and Treatment Hospital for Occupational Diseases, Chongqing, China.
Lianying ZhangThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Feiyu JiangThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Xiongmin MaoThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Gangyi YangChongqing Prevention and Treatment Hospital for Occupational Diseases, Chongqing, China.
Ling LiThe Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China. liling@cqmu.edu.cn.ORCID 0000-0002-0087-3034
Chongqing Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 21 (FGF21) plays an important role in regulating glucose and lipid metabolism, but its role in cancer is less well-studied. We aimed to investigate the action of FGF21 in the development of prostate cancer (PCa). Herein, we found that FGF21 expression was markedly downregulated in PCa tissues and cell lines. FGF21 inhibited the proliferation and clone formation of LNCaP cells (a PCa cell line) and promoted apoptosis. FGF21 also inhibited PCa cell migration and invasiveness. The Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that FGF21 was related to autophagy and the phosphatidylinositol 3-kinase-Akt kinase-mammalian target of rapamycin (PI3K-Akt-mTOR) pathway. Mechanistically, FGF21 promoted autophagy in LNCaP cells by inhibiting the PI3K-Akt-mTOR-70S6K pathway. In addition, FGF21 inhibited PCa tumorigenesis in vivo in nude mice. Altogether, our findings show that FGF21 inhibits PCa cell proliferation and promoted apoptosis in PCa cells through facilitated autophagy. Therefore, FGF21 might be a potential novel target in PCa therapy.

Indexed as

AnimalsAutophagyCell Line, TumorFibroblast Growth FactorsHeterograftsHumansMaleMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinaseProstatic NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTransfectionFGF21 protein, humanFibroblast Growth FactorsMTOR protein, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID33753729
PMCPMC7985321
OpenAlexW3138129058

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.