Evidence map›Paper›PMID 37041476›Full record

ArticleBMC cancer2023

SLC27A2 mediates FAO in colorectal cancer through nongenic crosstalk regulation of the PPARs pathway.

Kun Shang, Nina Ma, Juanjuan Che, Huihui Li, Jiexuan Hu, Haolin Sun, Bangwei Cao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 14 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

7 authors at 2 institutions in 1 country.

Kun ShangDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Nina MaDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Juanjuan CheDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Huihui LiDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Jiexuan HuDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Haolin SunDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China.
Bangwei CaoDepartment of Oncology, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xi-Cheng District, Beijing, 100050, China. oncology@ccmu.edu.cn.
Capital Medical University · CNBeijing Friendship Hospital · CN

Funding

Beijing Municipal Natural Science Foundation 7222032National Natural Science Foundation of China 82173056
6 · The paper itself

Abstract

backgroundPeroxisome proliferator activated receptors (PPARs) are a nuclear hormone receptors superfamily that is closely related to fatty acid (FA) metabolism and tumor progression. Solute carrier family 27 member 2 (SLC27A2) is important for FA transportation and metabolism and is related to cancer progression. This study aims to explore the mechanisms of how PPARs and SLC27A2 regulate FA metabolism in colorectal cancer (CRC) and find new strategies for CRC treatment.

methodsBiological information analysis was applied to detect the expression and the correlation of PPARs and SLC27A2 in CRC. The protein-protein interaction (PPI) interaction networks were explored by using the STRING database. Uptake experiments and immunofluorescence staining were used to analyse the function and number of peroxisomes and colocalization of FA with peroxisomes, respectively. Western blotting and qRT‒PCR were performed to explore the mechanisms.

resultsSLC27A2 was overexpressed in CRC. PPARs had different expression levels, and PPARG was significantly highly expressed in CRC. SLC27A2 was correlated with PPARs in CRC. Both SLC27A2 and PPARs were closely related to fatty acid oxidation (FAO)‒related genes. SLC27A2 affected the activity of ATP Binding Cassette Subfamily D Member 3 (ABCD3), also named PMP70, the most abundant peroxisomal membrane protein. We found that the ratios of p-Erk/Erk and p-GSK3β/GSK3β were elevated through nongenic crosstalk regulation of the PPARs pathway.

conclusionsSLC27A2 mediates FA uptake and beta-oxidation through nongenic crosstalk regulation of the PPARs pathway in CRC. Targeting SLC27A2/FATP2 or PPARs may provide new insights for antitumour strategies.

Indexed as

Colorectal NeoplasmsPeroxisome Proliferator-Activated ReceptorsCoenzyme A LigasesFatty AcidsGlycogen Synthase Kinase 3 betaHumansReceptors, Cytoplasmic and NuclearCoenzyme A LigasesFatty AcidsGlycogen Synthase Kinase 3 betaPeroxisome Proliferator-Activated ReceptorsReceptors, Cytoplasmic and NuclearColorectal cancerFAOPPARsSLC27A2

Identifiers

PMID37041476
PMCPMC10091540
OpenAlexW4364376278

What OpenQuestion holds

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LicenceCC BY
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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.