Evidence map›Paper›PMID 35130611›Full record

ArticleActa biochimica et biophysica Sinica2022

Overexpression CPT1A reduces lipid accumulation via PPARα/CD36 axis to suppress the cell proliferation in ccRCC.

Hui Yang, Hongbo Zhao, Zhongkun Ren, Xiaojia Yi, Qiao Zhang, Zhe Yang, Yingmin Kuang, Yuechun Zhu

Open access · greenAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-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

24 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

8 authors at 1 institution in 1 country.

Hui YangYunnan Key Laboratory of Stem Cell and Regenerative Medicine, Biomedical Engineering Research Center, Kunming Medical University, Kunming 650500, China.
Hongbo ZhaoYunnan Key Laboratory of Stem Cell and Regenerative Medicine, Biomedical Engineering Research Center, Kunming Medical University, Kunming 650500, China.
Zhongkun RenDepartment of Neurosurgery, the First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Xiaojia YiDepartment of Pathology, the Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China.
Qiao ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China.
Zhe YangDepartment of Pathology, the First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Yingmin KuangDepartment of Organ Transplantation, the First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Yuechun ZhuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China.
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clear cell renal carcinoma (ccRCC) is histologically defined by its cytoplasmic lipid deposits. Lipid metabolism disorder largely increases the risk of ccRCC. In this study, we aimed to investigate the biological functions and molecular mechanisms of carnitine palmitoyl transferase 1A (CPT1A) in ccRCC. Our results showed that CPT1A is decreased in ccRCC clinical samples and cell lines compared with that in normal samples. Lentivirus overexpressing CPT1A was used to investigate the neoplastic phenotypes of ccRCC, and the results showed that lipid accumulation and tumor growth are attenuated both and . In addition, CPT1A prevents cholesterol uptake and lipid accumulation by increasing the peroxisome proliferator-activated receptor α (PPARα) level through regulation of Class B scavenger receptor type 1 (SRB1) and cluster of differentiation 36 (CD36). Furthermore, PI3K/Akt signaling pathway promotes tumor cell proliferation in ccRCC, which is related to the enhanced expression of CD36. Functionally, weakened CPT1A expression is critical for lipid accumulation to promote ccRCC development. Collectively, our research unveiled a novel function of CPT1A in lipid metabolism via PPARα/CD36 axis, which provides a new theoretical explanation for the pathogenesis of ccRCC. Targeting CPT1A may be a potential therapeutic strategy to treat ccRCC.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsCarnitine O-PalmitoyltransferaseCell Line, TumorCell ProliferationHumansLipid MetabolismLipidsPhosphatidylinositol 3-KinasesPPAR alphaCarnitine O-PalmitoyltransferaseCPT1A protein, humanLipidsPhosphatidylinositol 3-KinasesPPAR alphaCD36cholesterolCPT1AgrowthPPARαrenal cancer

Identifiers

PMID35130611
PMCPMC9909300
OpenAlexW4205264351

What OpenQuestion holds

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LicenceCC BY-NC
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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.