Evidence map›Paper›PMID 36353618›Full record

ArticleFrontiers in immunology2022

Interaction of RARRES1 with ICAM1 modulates macrophages to suppress the progression of kidney renal clear cell carcinoma.

Xiaodong Geng, Kun Chi, Chao Liu, Zhangning Fu, Xu Wang, Liangliang Meng, Hanfeng Wang, Guangyan Cai, Xiangmei Chen, Quan Hong

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-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

9 citing papers in PubMed, 13 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

10 authors at 2 institutions in 1 country.

Xiaodong GengDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Kun ChiDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Chao LiuDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Zhangning FuDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Xu WangDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Liangliang MengDepartment of Radiology, First Medical Centre of Chinese People's Liberation Army (PLA) General Hospital, Beijing, China.
Hanfeng WangDepartment of Urology, Third Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Beijing, China.
Guangyan CaiDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Xiangmei ChenDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Quan HongDepartment of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing, China.
Chinese People's Liberation Army · CNState Key Laboratory of Kidney Diseases

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: RARRES1 is a tumor suppressor protein, and its expression is suppressed in various tumor cells. However, whether it participates in the immune response in kidney renal clear cell carcinoma (KIRC) is unknown, and the defined mechanism is not clear. Therefore, the mechanism of RARRES1 in KIRC is worthy of investigation. Methods: We analysed the expression and function of RARRES1 with The Cancer Genome Atlas (TCGA) database. The Kaplan-Meier curve was adopted to estimate survival. RARRES1-correlated genes were obtained from the UALCAN database and subjected to Gene Ontology (GO) enrichment and protein-protein interaction (PPI) network analyses. The correlation analysis between tumor-infiltrating immune cells and selected genes were performed with TIMER database. We also investigated the possible function of RARRES1 in KIRC by coculturing Caki-1 cells with THP-1 cells. Immunofluorescence assay was performed to study the RARRES1 expression in difference grade KIRC tissues. Results: The expression of RARRES1 was negatively correlated with survival in KIRC patients. The GO biological process term most significantly enriched with the RARRES1-correlated genes was regulation of cell adhesion. ICAM1, which exhibited a relatively highest correlation with RARRES1, is positively correlated with the infiltration level of macrophages. RARRES1 could enhance the expression of ICAM1 in Caki-1 cells and then induce the activation of M1 THP-1 cells to decrease the viability and induce the apoptosis of Caki-1 cells. Conclusion: RARRES1 plays an antitumor role by promoting ICAM1 expression and inducing the activation of M1 macrophages. We offer insights into the molecular mechanism of KIRC and reveal a potential therapeutic target.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsBiomarkers, TumorDatabases, GeneticGene Expression Regulation, NeoplasticHumansIntercellular Adhesion Molecule-1KidneyMacrophagesMembrane ProteinsPrognosisBiomarkers, TumorICAM1 protein, humanIntercellular Adhesion Molecule-1Membrane ProteinsRARRES1 protein, humanbioinformatic analysesICAM1kidney renal clear cell carcinomaM1 macrophagesRARRES1

Identifiers

PMID36353618
PMCPMC9638079
OpenAlexW4307156799

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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.