Evidence map›Paper›PMID 38684635›Full record

ArticlePhotochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology2024

Downregulation of SMAD4 protects HaCaT cells against UVB-induced damage and oxidative stress through the activation of EMT.

Xiangzhi Li, Yimeng Wang, Xian Wang, Yi Shen, Yawen Yuan, Qingquan He, Shuyi Mao, Cailian Wu, Meijuan Zhou

Abstract read
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In one paragraph

Article in Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Xiangzhi Li *Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China.
Yimeng Wang *Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China.
Xian Wang *Department of Public Health and Management, Youjiang Medical University for Nationalities, Baise, 533000, China.
Yi ShenDepartment of Public Health and Management, Youjiang Medical University for Nationalities, Baise, 533000, China.
Yawen YuanDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China.
Qingquan HeTaizhou Key Laboratory of Minimally Invasive Interventional Therapy & Artificial Intelligence, Taizhou Branch of Zhejiang Cancer Hospital (Taizhou Cancer Hospital), Taizhou, 317502, China.
Shuyi MaoNuclear Medicine Department, The Second Affiliated Hospital of Guangxi University of Science and Technology, Liuzhou, 545006, China.
Cailian WuDepartment of Public Health, School of Medicine, Guangxi University of Science and Technology, Liuzhou, 545000, China.
Meijuan ZhouDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China. lkzmj@smu.edu.cn.

Funding

Guangxi Zhuang Autonomous Region Health and Family Planning Commission Z20211580Innovative Research Group Project of the National Natural Science Foundation of China 31971167Innovative Research Group Project of the National Natural Science Foundation of China 82273582International Association for the Exchange of Students for Technical Experience 202110594024Liuzhou Science and Technology Project 2022CAC0229Science and Technology Program of Zhejiang Province 2024ZL1261
6 · The paper itself

Abstract

As a member of the SMAD family, SMAD4 plays a crucial role in several cellular biological processes. However, its function in UVB radiation-induced keratinocyte damage is not yet clarified. Our study aims to provide mechanistic insight for the development of future UVB protective therapies and therapeutics involving SMAD4. HaCaT cells were treated with UVB, and the dose dependence and time dependence of UVB were measured. The cell function of UVB-treated HaCaT cells and the activity of epithelial-mesenchymal transition (EMT) after overexpression or silencing of SMAD4 was observed by flow cytometry, quantitative reverse transcription PCR (qRT-PCR) and Western Blots (WB). We found that a significant decrease in SMAD4 was observed in HaCaT cells induced by UVB. Our data confirm SMAD4 as a direct downstream target of miR-664. The down-regulation of SMAD4 preserved the viability of the UVB-treated HaCaT cells by inhibiting autophagy or apoptosis. Furthermore, the silencing of SMAD4 activated the EMT process in UVB-treated HaCaT cells. Down-regulation of SMAD4 plays a protective role in UVB-treated HaCaT cells via the activation of EMT.

Indexed as

Epithelial-Mesenchymal TransitionSmad4 ProteinApoptosisCell SurvivalDown-RegulationHaCaT CellsHumansKeratinocytesOxidative StressUltraviolet RaysSmad4 ProteinSMAD4 protein, humanApoptosisAutophagyEMTSMAD4UVB

Identifiers

PMID38684635

What OpenQuestion holds

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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.