Evidence map›Paper›PMID 35307784›Full record

ArticleInflammation2022

CircOAS3 Regulates Keratinocyte Proliferation and Psoriatic Inflammation by Interacting with Hsc70 via the JNK/STAT3/NF-κB Signaling Pathway.

Zhenxian Yang, Xiran Yin, Cheng Chen, Shan Huang, Xueqing Li, Jianjun Yan, Qing Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

7 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 1 institution in 1 country.

Zhenxian YangDepartment of Dermatology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Xiran YinDepartment of Dermatology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Cheng ChenDepartment of Dermatology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Shan HuangDepartment of Dermatology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Xueqing LiDepartment of Dermatology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Jianjun YanDepartment of Dermatology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Qing SunDepartment of Dermatology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People's Republic of China. sunqing7226@163.com.ORCID http://orcid.org/0000-0003-3565-3530
Qilu Hospital of Shandong University · CN

Funding

National Major Science and Technology Projects of China Grant No. 2017YFA0104604National Natural Science Foundation of China Grant Nos.81972937National Natural Science Foundation of China Grant Nos.82003344
6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory disease of the skin with a very complex pathogenesis. Circular RNAs (circRNAs) play important regulatory roles in many diseases, including psoriasis. In this study, we found that circOAS3 expression was significantly upregulated in both psoriatic tissues and M5-induced keratinocytes. Silencing circOAS3 in HaCaT and Ker-CT cells inhibited their viability, promoted apoptosis, and blocked the cell cycle from the G1 to the S phase. RNA pull-down and RNA immunoprecipitation (RIP) analyses led to the identification of a direct interaction between circOAS3 and heat shock cognate protein 70 (Hsc70). Silencing circOAS3 expression negatively influenced Hsc70 protein expression but not mRNA expression. circOAS3 knockdown suppressed the activation of the JNK/STAT3/NF-κB signaling pathway. circOAS3 or Hsc70 silencing led to downregulated protein IL-6 expression, thus reducing psoriatic inflammation in vitro. In conclusion, the interaction between circOAS3 and Hsc70 mediates the proliferation and psoriatic inflammation of HaCaT and Ker-CT cells through the JNK/STAT3/NF-κB signaling pathway, suggesting that circOAS3 or Hsc70 may be a promising therapeutic target for psoriasis.

Indexed as

NF-kappa BPsoriasisCell ProliferationHSC70 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsHumansInflammationInterleukin-6KeratinocytesRNA, CircularSignal TransductionSTAT3 Transcription FactorHSC70 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsInterleukin-6NF-kappa BRNA, CircularSTAT3 protein, humanSTAT3 Transcription FactorcircOAS3Hsc70inflammation.proliferationpsoriasisRNA-binding protein

Identifiers

PMID35307784
OpenAlexW4221122718

What OpenQuestion holds

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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.