Evidence map›Paper›PMID 38017409›Full record

ArticleJournal of translational medicine2023

Identification and characterization of ARID1A-interacting proteins in renal tubular cells and their molecular regulation of angiogenesis.

Sunisa Yoodee, Paleerath Peerapen, Sirikanya Plumworasawat, Thanyalak Malaitad, Visith Thongboonkerd

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 10 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

5 authors at 1 institution in 1 country.

Sunisa YoodeeMedical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, 6thFloor - SiMR Building, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Paleerath PeerapenMedical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, 6thFloor - SiMR Building, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Sirikanya PlumworasawatMedical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, 6thFloor - SiMR Building, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Thanyalak MalaitadMedical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, 6thFloor - SiMR Building, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Visith ThongboonkerdMedical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, 6thFloor - SiMR Building, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand. thongboonkerd@dr.com.ORCID 0000-0001-7865-0765
Siriraj Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDefects and deficiency of AT-rich interactive domain-containing protein 1A (ARID1A) encoded by a tumor suppressor gene ARID1A have recently been suggested to get involved in angiogenesis, a crucial process in carcinogenesis. However, molecular mechanisms of ARID1A deficiency to induce angiogenesis in kidney cancer remain underinvestigated.

methodsWe performed large-scale identification of ARID1A protein interactors in renal tubular epithelial cells (RTECs) using immunoprecipitation (IP) followed by nanoLC-ESI-LTQ-Orbitrap tandem mass spectrometry (MS/MS). Their roles in angiogenesis were investigated using various assays.

resultsA total of 74 ARID1A-interacting proteins were identified. Protein-protein interactions analysis revealed that these identified proteins interacted directly or indirectly with ARID1A. Among them, the direct interaction between ARID1A and β-actin was validated by IP and reciprocal IP followed by Western blotting. Small interfering RNA (siRNA) was used for single and double knockdowns of ARID1A and ACTB. Semi-quantitative RT-PCR demonstrated that deficiency of ARID1A, but not ACTB, significantly affected expression of angiogenesis-related genes in RTECs (VEGF and FGF2 were increased, whereas PDGF and EGF were decreased). However, the knockdowns did not affect TGFB1 and FGF1 levels. The quantitative mRNA expression data of VEGF and TGFB1 were consistent with the secreted levels of their protein products as measured by ELISA. Only secreted products derived from ARID1A-deficient RTECs significantly increased endothelial cells (ECs) migration and tube formation. Some of the other carcinogenic features could also be confirmed in the ARID1A-deficient RTECs, including increased cell migration and chemoresistance. Double knockdowns of both ARID1A and ACTB did not enhance the effects of single ARID1A knockdown in all assays.

conclusionsWe report herein a large dataset of the ARID1A-interacting proteins in RTECs using an IP-MS/MS approach and confirm the direct interaction between ARID1A and β-actin. However, the role of ARID1A deficiency in angiogenesis is independent of β-actin.

Indexed as

ActinsKidney NeoplasmsDNA-Binding ProteinsEndothelial CellsEpithelial CellsHumansNuclear ProteinsRNA, Small InterferingTandem Mass SpectrometryTranscription FactorsVascular Endothelial Growth Factor AActinsARID1A protein, humanDNA-Binding ProteinsNuclear ProteinsRNA, Small InterferingTranscription FactorsVascular Endothelial Growth Factor AActinEndothelial cellsInteracting proteinsRenal cancerRenal epithelial cellsTumor suppressor

Identifiers

PMID38017409
PMCPMC10683333
OpenAlexW4389079376

What OpenQuestion holds

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LicenceCC BY
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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.