Evidence map›Paper›PMID 30931936›Full record

ArticleCell death & disease2019

USF1-induced upregulation of LINC01048 promotes cell proliferation and apoptosis in cutaneous squamous cell carcinoma by binding to TAF15 to transcriptionally activate YAP1.

Lezi Chen, Quan Chen, Shifeng Kuang, Chengli Zhao, Lu Yang, Yi Zhang, Huilan Zhu, Ridong Yang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

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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

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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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  6. Epigenetics · 2024
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  8. Article
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  11. Article
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  15. Review
  16. Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
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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

8 authors at 4 institutions in 1 country.

Lezi ChenDepartment of Plastic and Peripheral Vascular Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences., 106, Zhongshan 2nd Road, Guangzhou, 510080, Guangdong, China.
Quan ChenGuangzhou Institute of Dermatology, Institute of Dermatology, Guangzhou Medical University, No.56 Hengfu Road, Guangzhou, 510095, Guangdong, China.
Shifeng KuangDepartment of Plastic and Peripheral Vascular Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences., 106, Zhongshan 2nd Road, Guangzhou, 510080, Guangdong, China. 306275883@qq.com.
Chengli ZhaoDepartment of Plastic and Peripheral Vascular Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences., 106, Zhongshan 2nd Road, Guangzhou, 510080, Guangdong, China.
Lu YangDepartment of Plastic and Peripheral Vascular Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences., 106, Zhongshan 2nd Road, Guangzhou, 510080, Guangdong, China.
Yi ZhangDepartment of Plastic and Peripheral Vascular Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences., 106, Zhongshan 2nd Road, Guangzhou, 510080, Guangdong, China.
Huilan ZhuGuangzhou Institute of Dermatology, Institute of Dermatology, Guangzhou Medical University, No.56 Hengfu Road, Guangzhou, 510095, Guangdong, China.
Ridong YangGuangzhou Institute of Dermatology, Institute of Dermatology, Guangzhou Medical University, No.56 Hengfu Road, Guangzhou, 510095, Guangdong, China. Yrdgz63@gmail.com.
Guangdong General Hospital · CNGuangdong Academy of Medical Sciences · CNGuangzhou Institute of Dermatology · CNGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have revealed that dysregulation of long non-coding RNAs (lncRNAs) can facilitate carcinogenesis. This study aims to investigate the biological role of a certain lncRNA in cutaneous squamous cell carcinoma (CSCC). According to the data of TCGA database, high expression of long intergenic non-protein coding RNA 1048 (LINC01048) is an unfavorable prognostic factor for patients with CSCC. Therefore, we further detected the expression pattern of LINC01048 in CSCC tissues. Obviously, LINC01048 was expressed higher in the CSCC tissues and recurrence tissues compared with that in adjacent normal tissues and non-recurrence tissues. Furthermore, Kaplan-Meier analysis revealed the negative correlation between LINC01048 expression and the overall survival and disease-free survival of CSCC patients. Subsequently, functional assays were conducted to prove the inhibitory effect of silenced LINC01048 on the proliferation and apoptosis of CSCC cells. Mechanistically, LINC01048 was proved to be transcriptionally activated by USF1. Pathway analysis and western blot assay showed that knockdown of LINC01048 led to the activation of Hippo pathway. Moreover, YAP1, a Hippo pathway factor, was positively regulated by LINC01048. Further mechanism investigation revealed that LINC01048 increased the binding of TAF15 to YAP1 promoter to transcriptionally activate YAP1 in CSCC cells. Finally, rescue assays demonstrated that YAP1 involved in LINC01048-mediated CSCC cell proliferation and apoptosis. In conclusion, USF1-induced upregulation of LINC01048 promoted CSCC by interacting with TAF15 to upregulate YAP1.

Indexed as

Adaptor Proteins, Signal TransducingAmino Acid MotifsAnimalsApoptosisCarcinoma, Squamous CellCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudePrognosisPromoter Regions, GeneticRNA, Long NoncodingSignal TransductionAdaptor Proteins, Signal TransducingRNA, Long NoncodingTAF15 protein, humanTATA-Binding Protein Associated FactorsTranscription FactorsUpstream Stimulatory FactorsUSF1 protein, humanYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID30931936
PMCPMC6443651
OpenAlexW2929890290

What OpenQuestion holds

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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.