Evidence map›Paper›PMID 32541839›Full record

ArticleOncogene2020

Iron chelation inhibits mTORC1 signaling involving activation of AMPK and REDD1/Bnip3 pathways.

Chaowei Shang, Hongyu Zhou, Wang Liu, Tao Shen, Yan Luo, Shile Huang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Iron dysregulation in the central nervous system: implications for autism spectrum disorder.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  10. Spns1 is an iron transporter essential for megalin-dependent endocytosis.American journal of physiology. Renal physiology · 2024
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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

6 authors at 1 institution in 1 country.

Chaowei Shang *Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA.
Hongyu Zhou *Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA.
Wang Liu *Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA.
Tao ShenDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA.
Yan LuoDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA.
Shile HuangDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71130-3932, USA. shuan1@lsuhsc.edu.ORCID http://orcid.org/0000-0002-3239-1072
Louisiana State University Health Sciences Center Shreveport · US

Funding

mTOR Signaling in Tumor Cell MotilityR01CA115414 · NCI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI HUANG, SHILE · 2006 to 2009
$811k
NCI NIH HHS R01 CA115414
6 · The paper itself

Abstract

The mammalian target of rapamycin (mTOR) functions as two complexes (mTORC1 and mTORC2), regulating cell growth and metabolism. Aberrant mTOR signaling occurs frequently in cancers, so mTOR has become an attractive target for cancer therapy. Iron chelators have emerged as promising anticancer agents. However, the mechanisms underlying the anticancer action of iron chelation are not fully understood. Particularly, reports on the effects of iron chelation on mTOR complexes are inconsistent or controversial. Here, we found that iron chelators consistently inhibited mTORC1 signaling, which was blocked by pretreatment with ferrous sulfate. Mechanistically, iron chelation-induced mTORC1 inhibition was not related to ROS induction, copper chelation, or PP2A activation. Instead, activation of AMPK pathway mainly and activation of both HIF-1/REDD1 and Bnip3 pathways partially contribute to iron chelation-induced mTORC1 inhibition. Our findings indicate that iron chelation inhibits mTORC1 via multiple pathways and iron is essential for mTORC1 activation.

Indexed as

AMP-Activated Protein KinasesCell Line, TumorHumansIron Chelating AgentsMembrane ProteinsProto-Oncogene ProteinsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesBNIP3 protein, humanIron Chelating AgentsMembrane ProteinsMTOR protein, humanProto-Oncogene ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID32541839
PMCPMC7366895
OpenAlexW3034308531

What OpenQuestion holds

Textmetadata
LicenceTDM
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.