3-Deoxysappanchalcone Inhibits Skin Cancer Proliferation by Regulating T-Lymphokine-Activated Killer Cell-Originated Protein Kinase
3-deoxysappanchalcone
T-LAK cell-originated protein kinase
cancer growth
skin cancer
skin hyperplasia
solar sinulated light
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2021
2021
Historique:
received:
05
12
2020
accepted:
16
02
2021
entrez:
12
4
2021
pubmed:
13
4
2021
medline:
13
4
2021
Statut:
epublish
Résumé
Skin cancer is one of the most commonly diagnosed cancers worldwide. The 5-year survival rate of the most aggressive late-stage skin cancer ranges between 20 and 30%. Thus, the discovery and investigation of novel target therapeutic agents that can effectively treat skin cancer is of the utmost importance. The T-lymphokine-activated killer cell-originated protein kinase (TOPK), which belongs to the serine-threonine kinase class of the mitogen-activated protein kinase kinase (MAPKK) family, is highly expressed and activated in skin cancer. The present study investigates the role of 3-deoxysappanchalcone (3-DSC), a plant-derived functional TOPK inhibitor, in suppressing skin cancer cell growth. In the context of skin cancer prevention and therapy, we clarify the effect and mechanism of 3-DSC on different types of skin cancer and solar-simulated light (SSL)-induced skin hyperplasia. In an 3-DSC is able to inhibit cell proliferation in skin cancer cells in an anchorage-dependent and anchorage-independent manner by regulation of TOPK and its related signaling pathway Our results suggest that 3-DSC may function in a chemopreventive and chemotherapeutic capacity by protecting against UV-induced skin hyperplasia and inhibiting tumor cell growth by attenuating TOPK signaling, respectively.
Sections du résumé
BACKGROUND
BACKGROUND
Skin cancer is one of the most commonly diagnosed cancers worldwide. The 5-year survival rate of the most aggressive late-stage skin cancer ranges between 20 and 30%. Thus, the discovery and investigation of novel target therapeutic agents that can effectively treat skin cancer is of the utmost importance. The T-lymphokine-activated killer cell-originated protein kinase (TOPK), which belongs to the serine-threonine kinase class of the mitogen-activated protein kinase kinase (MAPKK) family, is highly expressed and activated in skin cancer. The present study investigates the role of 3-deoxysappanchalcone (3-DSC), a plant-derived functional TOPK inhibitor, in suppressing skin cancer cell growth.
PURPOSE
OBJECTIVE
In the context of skin cancer prevention and therapy, we clarify the effect and mechanism of 3-DSC on different types of skin cancer and solar-simulated light (SSL)-induced skin hyperplasia.
METHODS
METHODS
In an
RESULTS
RESULTS
3-DSC is able to inhibit cell proliferation in skin cancer cells in an anchorage-dependent and anchorage-independent manner by regulation of TOPK and its related signaling pathway
CONCLUSIONS
CONCLUSIONS
Our results suggest that 3-DSC may function in a chemopreventive and chemotherapeutic capacity by protecting against UV-induced skin hyperplasia and inhibiting tumor cell growth by attenuating TOPK signaling, respectively.
Identifiants
pubmed: 33842463
doi: 10.3389/fcell.2021.638174
pmc: PMC8027363
doi:
Types de publication
Journal Article
Langues
eng
Pagination
638174Informations de copyright
Copyright © 2021 Fu, Zhao, Yoon, Shim, Choi, Yin, Xu, Laster, Liu, Dong and Lee.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Biochem Biophys Res Commun. 2020 Jan 29;522(1):270-277
pubmed: 31757421
J Neurosci. 2005 Nov 16;25(46):10773-85
pubmed: 16291951
PLoS Biol. 2018 Sep 27;16(9):e2006624
pubmed: 30261040
Oncotarget. 2017 Jun 20;8(25):40190-40203
pubmed: 28212583
Neuropathology. 2018 Jun;38(3):228-236
pubmed: 29575092
EBioMedicine. 2017 Apr;18:73-82
pubmed: 28412249
Cell Death Dis. 2018 Oct 24;9(11):1089
pubmed: 30356039
J Biol Chem. 2000 Jul 14;275(28):21525-31
pubmed: 10781613
Cancer Res. 2012 Jun 15;72(12):3060-8
pubmed: 22523035
Oncogene. 2018 Oct;37(42):5633-5647
pubmed: 29904102
Cancers (Basel). 2019 Oct 22;11(10):
pubmed: 31652660
Gastroenterology. 2007 Jul;133(1):219-31
pubmed: 17631144
Br J Pharmacol. 2020 May;177(10):2303-2319
pubmed: 31985814
Cancer Prev Res (Phila). 2015 Aug;8(8):720-8
pubmed: 26031292
Cell Death Dis. 2019 Feb 18;10(3):166
pubmed: 30778048
Oncotarget. 2016 May 3;7(18):26604-16
pubmed: 27049917
Phytomedicine. 2019 Aug;61:152813
pubmed: 31035049
Br J Cancer. 2017 Aug 8;117(4):503-512
pubmed: 28677687
Oncogene. 2010 Oct 7;29(40):5464-74
pubmed: 20622899
Cancer Res. 2006 Sep 15;66(18):9186-95
pubmed: 16982762
Oncotarget. 2016 Feb 9;7(6):6748-64
pubmed: 26745678
Neuropathology. 2018 Apr;38(2):144-153
pubmed: 29271010
Mol Cancer Ther. 2017 Sep;16(9):1843-1854
pubmed: 28655782
MAbs. 2018 Nov-Dec;10(8):1301-1311
pubmed: 30204048
J Cancer. 2019 Jan 1;10(1):131-137
pubmed: 30662533
Hum Pathol. 2015 Feb;46(2):217-24
pubmed: 25466965
Cell Death Dis. 2019 Oct 14;10(10):777
pubmed: 31611604
Anticancer Res. 2016 Dec;36(12):6457-6466
pubmed: 27919968
Oncotarget. 2015 Oct 20;6(32):33410-25
pubmed: 26450903
BMC Cancer. 2019 Dec 30;19(1):1264
pubmed: 31888532
J Cell Physiol. 2019 Jan 29;:
pubmed: 30697722
PLoS One. 2018 Oct 4;13(10):e0204866
pubmed: 30286126
Medicine (Baltimore). 2019 Mar;98(10):e14766
pubmed: 30855480
Sci Transl Med. 2014 Oct 22;6(259):259ra145
pubmed: 25338756
Br J Cancer. 2017 Jan 17;116(2):218-226
pubmed: 27898655
Oncotarget. 2017 Apr 18;8(16):27093-27104
pubmed: 28404919
Histopathology. 2013 Nov;63(5):696-703
pubmed: 24025073
Clin Cancer Res. 2016 Dec 15;22(24):6110-6117
pubmed: 27334838
J Clin Invest. 2012 Feb;122(2):464-72
pubmed: 22293185
Int Immunopharmacol. 2014 Oct;22(2):420-6
pubmed: 25091623
Prim Care. 2015 Dec;42(4):645-59
pubmed: 26612377