Evidence map›Paper›PMID 34431227›Full record

ArticleJournal of cellular and molecular medicine2021

CCAT1/FABP5 promotes tumour progression through mediating fatty acid metabolism and stabilizing PI3K/AKT/mTOR signalling in lung adenocarcinoma.

Jing Chen, Yaser Alduais, Kai Zhang, Xiaoli Zhu, Baoan Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

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  13. USP14 targets FABP5-mediated ferroptosis to promote proliferation and cisplatin resistance of HNSCC.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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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

5 authors at 2 institutions in 1 country.

Jing ChenDepartment of Hematology and Oncology, School of Medicine, Zhongda Hospital, Southeast University, Nanjing, China.ORCID 0000-0001-9776-9470
Yaser AlduaisDepartment of Hematology and Oncology, School of Medicine, Zhongda Hospital, Southeast University, Nanjing, China.
Kai ZhangDepartment of Respiratory Medicine, Nanjing First Hospital, Nanjing, China.
Xiaoli ZhuDepartment of Respiratory Medicine, School of Medicine, Zhongda Hospital, Southeast University, Nanjing, China.
Baoan ChenDepartment of Hematology and Oncology, School of Medicine, Zhongda Hospital, Southeast University, Nanjing, China.
Zhongda Hospital Southeast University · CNNanjing Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) colon cancer associated transcript 1 (CCAT1) has been identified as an oncogene in many cancers, but its role in lung adenocarcinoma (LUAD) remains to be further investigated. We identified the upregulation of CCAT1 in LUAD tissues and LUAD cells. Through RNA pull-down and mass spectrometry analysis, we obtained the interacting proteins with CCAT1 and discovered their functional relation with 'signal transduction', 'energy pathways' and 'metabolism' and revealed the potential of CCAT1 on fatty acid (FA) metabolism. For mechanism exploration, we uncovered the mediation of CCAT1 on the translocation of fatty acid binding protein 5 (FABP5) into nucleus by confirming their interaction and localization. Also, CCAT1 was discovered to promote the formation of the transcription complex by RXR and PPARγ so as to activate the transcription of CD36, PDK1 and VEGFA. Moreover, we found that CCAT1 regulated the activity of AKT by promoting the ubiquitination of FKBP51 through binding with USP49. Subsequently, cell function assays revealed the enhancement of CCAT1 on LUAD cell proliferation and angiogenesis in vitro and in vivo. Collectively, CCAT1 regulated cell proliferation and angiogenesis through regulating FA metabolism in LUAD, providing a novel target for LUAD treatment.

Indexed as

Signal TransductionAdenocarcinoma of LungAnimalsCell Line, TumorDisease Models, AnimalDisease ProgressionFatty Acid-Binding ProteinsFatty AcidsHeterograftsHumansLipid MetabolismMiceModels, BiologicalNeovascularization, PathologicPhosphatidylinositol 3-KinasesProtein BindingCCAT1 long noncoding RNA, humanFABP5 protein, humanFatty Acid-Binding ProteinsFatty AcidsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA-Binding ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesangiogenesisCCAT1fatty acid metabolismlung adenocarcinomaubiquitination

Identifiers

PMID34431227
PMCPMC8500980
OpenAlexW3195266229

What OpenQuestion holds

Textmetadata
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.