Evidence map›Paper›PMID 37642779›Full record

ArticleCellular and molecular life sciences : CMLS2023

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness.

Shanchun Guo, Vanajothi Ramar, Alyssa A Guo, Talib Saafir, Hannah Akpobiyeri, Breanna Hudson, Jason Li, Mingli Liu

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.5field-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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Multi-omics analysis identifieTranslational cancer research · 2026
    Article
  2. Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  3. Article
  4. Article
  5. Recent Advances in the Application of Cucurbitacin B as an Anticancer Agent.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024
    Article
  13. Review
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

8 authors at 4 institutions in 1 country.

Shanchun GuoDepartment of Chemistry, Xavier University, 1 Drexel Dr, New Orleans, LA, USA.
Vanajothi RamarDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, USA.
Alyssa A GuoUniversity of South Carolina SOM Greenville, Greenville, SC, USA.
Talib SaafirDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, USA.
Hannah AkpobiyeriDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, USA.
Breanna HudsonDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, USA.
Jason LiWake Forest University School of Medicine, 475 Vine Street, Winston-Salem, NC, USA.
Mingli LiuDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, USA. mliu@msm.edu.ORCID http://orcid.org/0000-0002-0052-0503
Morehouse School of Medicine · USUniversity of South Carolina · USWake Forest University · USXavier University · US

Funding

TRPM7 induces tumorigenesis and stemness through Notch activation in gliomaSC1GM144021 · NIGMS · MOREHOUSE SCHOOL OF MEDICINE · PI LIU, MINGLI · 2022 to 2025
$1.4M
NIGMS NIH HHS SC1 GM144021
6 · The paper itself

Abstract

introductionWe previously reported that TRPM7 regulates glioma cells' stemness through STAT3. In addition, we demonstrated that FOSL1 is a response gene for TRPM7, and the FOSL1 gene serves as an oncogene to promote glioma proliferation and invasion.

methodsIn the present study, we determined the effects of FOSL1 on glioma stem cell (GSC) markers CD133 and ALDH1 by flow cytometry, and the maintenance of stem cell activity by extreme limiting dilution assays (ELDA). To further gain insight into the mechanism by which TRPM7 activates transcription of the FOSL1 gene to contribute to glioma stemness, we constructed a FOSL1 promoter and its GAS mutants followed by luciferase reporter assays and ChIP-qPCR in a glioma cell line and glioma patient-derived xenoline. We further examined GSC markers ALDH1 and TRPM7 as well as FOSL1 by immunohistochemistry staining (IHC) in brain tissue microarray (TMA) of glioma patients.

resultsWe revealed that FOSL1 knockdown reduces the expression of GSC markers CD133 and ALDH1, and FOSL1 is required to maintain stem cell activity in glioma cells. The experiments also showed that mutations of - 328 to - 336 and - 378 to - 386 GAS elements markedly reduced FOSL1 promoter activity. Constitutively active STAT3 increased while dominant-negative STAT3 decreased FOSL1 promoter activity. Furthermore, overexpression of TRPM7 enhanced while silencing of TRPM7 reduced FOSL1 promoter activity. ChIP-qPCR assays revealed that STAT3, present in nuclear lysates of glioma cells stimulated by constitutively activated STAT3, can bind to two GAS elements, respectively. We demonstrated that deacetylation of FOSL1 at the Lys-116 residue located within its DNA binding domain led to an increase in FOSL1 transcriptional activity. We found that the expression of TRPM7, ALDH1, and FOSL1 protein is associated with grades of malignant glioma, and TRPM7 protein expression correlates to the expression of ALDH1 and FOSL1 in glioma patients.

conclusionsThese combined results demonstrated that TRPM7 induced FOSL1 transcriptional activation, which is mediated by the action of STAT3, a mechanism shown to be important in glioma stemness. These results indicated that FOSL1, similar to GSC markers ALDH1 and TRPM7, is a diagnostic marker and potential drug target for glioma patients.

Indexed as

GliomaTRPM Cation ChannelsBiological AssayBrainHumansOncogenesProtein Serine-Threonine KinasesSTAT3 Transcription FactorProtein Serine-Threonine KinasesSTAT3 protein, humanSTAT3 Transcription FactorTRPM7 protein, humanTRPM Cation ChannelsFOSL1GliomaGlioma stem cellsSignaling pathwaysSTAT3TRPM7

Identifiers

PMID37642779
PMCPMC10465393
OpenAlexW4386246047

What OpenQuestion holds

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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.