Evidence map›Paper›PMID 30755372›Full record

ArticleEBioMedicine2019

Inhibition of oncogenic Src induces FABP4-mediated lipolysis via PPARγ activation exerting cancer growth suppression.

Tuyen N M Hua, Min-Kyu Kim, Vu T A Vo, Jong-Whan Choi, Jang Hyun Choi, Hyun-Won Kim, Seung-Kuy Cha, Kyu-Sang Park, Yangsik Jeong

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Frontiers in oncology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025
    Review
  7. PGC-1α Activation by Polyphenols: A Pathway to Thermogenesis.Molecular nutrition & food research · 2025
    Review
  8. Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
    Article
  9. Review
  10. Article
  11. Green SeaweedMarine drugs · 2024
    Article
  12. Dual function of activated PPARγ by ligands on tumor growth and immunotherapy.Medical oncology (Northwood, London, England) · 2024
    Review
  13. Review
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  15. Article
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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 1 institution in 1 country.

Tuyen N M HuaDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Min-Kyu KimDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Vu T A VoDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Jong-Whan ChoiDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Jang Hyun ChoiDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 689-798, Republic of Korea.
Hyun-Won KimDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Seung-Kuy ChaDepartment of Physiology, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Lifestyle Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Mitochondrial Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Nuclear Receptor Research Consortium, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Kyu-Sang ParkDepartment of Physiology, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Lifestyle Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Mitochondrial Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea.
Yangsik JeongDepartment of Biochemistry, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Mitohormesis Research Center, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Lifestyle Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Institute of Mitochondrial Medicine, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea; Nuclear Receptor Research Consortium, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do 26426, Republic of Korea. Electronic address: yjeong@yonsei.ac.kr.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundc-Src is a driver oncogene well-known for tumorigenic signaling, but little for metabolic function. Previous reports about c-Src regulation of glucose metabolism prompted us to investigate its function in other nutrient modulation, particularly in lipid metabolism.

methodsOil-red O staining, cell growth assay, and tumor volume measurement were performed to determine lipid amount and growth inhibitory effect of treatments in lung cancer cells and xenograft model. Gene expression was evaluated by immunoblotting and relative RT-PCR. Transcriptional activity of peroxisome proliferator-activated receptor gamma (PPARγ) was assessed by luciferase assay. Reactive oxygen species (ROS) was measured using ROS sensing dye. Oxygen consumption rate was evaluated by Seahorse XF Mito Stress Test. Clinical relevance of candidate proteins was examined using patient samples and public database analysis.

findingsInhibition of Src induced lipolysis and increased intracellular ROS. Src inhibition derepressed PPARγ transcriptional activity leading to induced expression of lipolytic gene fatty acid binding protein (FABP) 4 which accompanies reduced lipid droplets and decreased tumor growth. The reverse correlation of Src and FABP4 was confirmed in pair-matched lung cancer patient samples, and further analysis using public datasets revealed upregulation of lipolytic genes is associated with better prognosis of cancer patients.

interpretationThis study provides an insight of how oncogenic factor Src concurrently regulates both cellular signaling pathways and metabolic plasticity to drive cancer progression. FUND: National Research Foundation of Korea and Korea Health Industry Development Institute.

Indexed as

LipolysisAnimalsAntineoplastic AgentsCell Line, TumorCSK Tyrosine-Protein KinaseFatty Acid-Binding ProteinsHEK293 CellsHumansIndolesLung NeoplasmsMiceMice, Inbred BALB CMice, NudePPAR gammaProtein Kinase InhibitorsReactive Oxygen SpeciesAntineoplastic AgentsCSK protein, humanCSK Tyrosine-Protein KinaseFabp4 protein, mouseFatty Acid-Binding ProteinsIndolesPPAR gammaProtein Kinase InhibitorsReactive Oxygen Speciessrc-Family KinasesSU 6656SulfonamidesFABP4LipidLung cancerPPARγSrc

Identifiers

PMID30755372
PMCPMC6442332
OpenAlexW2911512149

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.