Evidence map›Paper›PMID 37287005›Full record

ArticleCell & bioscience2023

FFAR2 antagonizes TLR2- and TLR3-induced lung cancer progression via the inhibition of AMPK-TAK1 signaling axis for the activation of NF-κB.

Mi-Jeong Kim, Ji Young Kim, Ji Hye Shin, Yeeun Kang, Ji Su Lee, Juhee Son, Soo-Kyung Jeong, Daesik Kim, Duk-Hwan Kim, Eunyoung Chun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Mi-Jeong Kim *Department of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Ji Young Kim *Department of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Ji Hye Shin *Department of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Yeeun KangDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Ji Su LeeDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Juhee SonDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Soo-Kyung JeongR&D Center, CHA Vaccine Institute, Seongnam-si, 13493, Republic of Korea.
Daesik KimDepartment of Precision Medicine, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Duk-Hwan KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Eunyoung ChunR&D Center, CHA Vaccine Institute, Seongnam-si, 13493, Republic of Korea. echun@chamc.co.kr.
Ki-Young LeeDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea. thylee@skku.edu.ORCID http://orcid.org/0000-0002-6722-1751
Samsung (South Korea) · KRCHA Vaccine Institute (South Korea) · KRSungkyunkwan University · KRSamsung Medical Center · KR

Funding

National Research Foundation of Korea NRF-2021R1A2C1094478
6 · The paper itself

Abstract

backgroundFree fatty acid receptors (FFARs) and toll-like receptors (TLRs) recognize microbial metabolites and conserved microbial products, respectively, and are functionally implicated in inflammation and cancer. However, whether the crosstalk between FFARs and TLRs affects lung cancer progression has never been addressed.

methodsWe analyzed the association between FFARs and TLRs using The Cancer Genome Atlas (TCGA) lung cancer data and our cohort of non-small cell lung cancer (NSCLC) patient data (n = 42), and gene set enrichment analysis (GSEA) was performed. For the functional analysis, we generated FFAR2-knockout (FFAR2KO) A549 and FFAR2KO H1299 human lung cancer cells and performed biochemical mechanistic studies and cancer progression assays, including migration, invasion, and colony-formation assays, in response to TLR stimulation.

resultsThe clinical TCGA data showed a significant down-regulation of FFAR2, but not FFAR1, FFAR3, and FFAR4, in lung cancer, and a negative correlation with TLR2 and TLR3. Notably, GSEA showed significant enrichment in gene sets related to the cancer module, the innate signaling pathway, and the cytokine-chemokine signaling pathway in FFAR2

conclusionOur results suggest that FFAR2 signaling antagonized TLR2- and TLR3-induced lung cancer progression via the suppression of the cAMP-AMPK-TAK1 signaling axis for the activation of NF-κB, and its agonist might be a potential therapeutic agent for the treatment of lung cancer.

Indexed as

FFAR2Lung cancer progressionNF-κBSCFAsToll-like receptors

Identifiers

PMID37287005
PMCPMC10249240
OpenAlexW4379741598

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.