Evidence map›Paper›PMID 33664254›Full record

ArticleCell death & disease2021

Loss of retinoic acid receptor-related receptor alpha (Rorα) promotes the progression of UV-induced cSCC.

Guolong Zhang, Guorong Yan, Zhiliang Fu, Yuhao Wu, Fei Wu, Zhe Zheng, Shan Fang, Ying Gao, Xunxia Bao, Yeqiang Liu and 2 more

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

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-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

12 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

12 authors at 2 institutions in 1 country.

Guolong Zhang *Institute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.ORCID 0000-0002-9207-1361
Guorong Yan *Institute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.ORCID 0000-0001-9200-2959
Zhiliang FuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Yuhao WuInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.
Fei WuDepartment of Pathology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.
Zhe ZhengInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.
Shan FangInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.
Ying GaoInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China.
Xunxia BaoState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.ORCID 0000-0002-6085-7319
Yeqiang LiuDepartment of Pathology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China. lyqdoctor@163.com.ORCID 0000-0003-3758-1390
Xiuli WangInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, 200443, China. wangxiuli_1400023@tongji.edu.cn.ORCID 0000-0002-0722-1274
Sibo ZhuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China. sibozhu@fudan.edu.cn.ORCID 0000-0003-4800-8987
Tongji University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cutaneous squamous cell carcinoma (cSCC) is prevalent in the world, accounting for a huge part of non-melanoma skin cancer. Most cSCCs are associated with a distinct pre-cancerous lesion, the actinic keratosis (AK). However, the progression trajectory from normal skin to AK and cSCC has not been fully demonstrated yet. To identify genes involved in this progression trajectory and possible therapeutic targets for cSCC, here we constructed a UV-induced cSCC mouse model covering the progression from normal skin to AK to cSCC, which mimicked the solar UV radiation perfectly using the solar-like ratio of UVA and UVB, firstly. Then, transcriptome analysis and a series of bioinformatics analyses and cell experiments proved that Rorα is a key transcript factor during cSCC progression. Rorα could downregulate the expressions of S100a9 and Sprr2f in cSCC cells, which can inhibit the proliferation and migration in cSCC cells, but not the normal keratinocyte. Finally, further animal experiments confirmed the inhibitory effect of cSCC growth by Rorα in vivo. Our findings showed that Rorα would serve as a potential novel target for cSCC, which will facilitate the treatment of cSCC in the future.

Indexed as

AnimalsCalgranulin BCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticCornified Envelope Proline-Rich ProteinsDisease Models, AnimalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansKeratosis, ActinicMiceMice, HairlessCalgranulin BCornified Envelope Proline-Rich ProteinsNuclear Receptor Subfamily 1, Group F, Member 1Octamer Transcription FactorsPOU2F3 protein, humanPou2f3 protein, mouseRORA protein, humanRora protein, mouseS100A9 protein, humanS100A9 protein, mouseSPRR2F protein, humanSprr2f protein, mouse

Identifiers

PMID33664254
PMCPMC7933246
OpenAlexW3133808667

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.