Shikonin derivatives cause apoptosis and cell cycle arrest in human chondrosarcoma cells via death receptors and MAPK regulation.
Acetylshikonin
Apoptosis
Chondrosarcoma
Cyclopropylshikonin
Death receptors
MAPK signaling
Shikonin
Journal
BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800
Informations de publication
Date de publication:
12 Jul 2022
12 Jul 2022
Historique:
received:
04
05
2022
accepted:
05
07
2022
entrez:
12
7
2022
pubmed:
13
7
2022
medline:
15
7
2022
Statut:
epublish
Résumé
Although chondrosarcoma is the second most common primary malignant bone tumor, treatment options are limited due to its extensive resistance to a chemo- and radiation therapy. Since shikonin has shown potent anticancer activity in various types of cancer cells, it represents a promising compound for the development of a new therapeutic approach. The dose-relationships of shikonin and its derivatives acetylshikonin and cyclopropylshikonin on two human chondrosarcoma cell lines were measured using the CellTiter-Glo®. The changes in the cell cycle were presented by flow cytometry. Protein phosphorylation and expression apoptotic markers, MAPKs and their downstream targets were analyzed using western blotting and gene expression were evaluated using RT-qPCR. Chondrosarcoma cells showed a dose-dependent inhibition of cell viability after treatment with shikonin and its derivatives, with the strongest effect for shikonin and IC These data demonstrated the significant anti-tumorigenic effect of shikonin derivatives in chondrosarcoma and encourage further research.
Sections du résumé
BACKGROUND
BACKGROUND
Although chondrosarcoma is the second most common primary malignant bone tumor, treatment options are limited due to its extensive resistance to a chemo- and radiation therapy. Since shikonin has shown potent anticancer activity in various types of cancer cells, it represents a promising compound for the development of a new therapeutic approach.
METHODS
METHODS
The dose-relationships of shikonin and its derivatives acetylshikonin and cyclopropylshikonin on two human chondrosarcoma cell lines were measured using the CellTiter-Glo®. The changes in the cell cycle were presented by flow cytometry. Protein phosphorylation and expression apoptotic markers, MAPKs and their downstream targets were analyzed using western blotting and gene expression were evaluated using RT-qPCR.
RESULTS
RESULTS
Chondrosarcoma cells showed a dose-dependent inhibition of cell viability after treatment with shikonin and its derivatives, with the strongest effect for shikonin and IC
CONCLUSIONS
CONCLUSIONS
These data demonstrated the significant anti-tumorigenic effect of shikonin derivatives in chondrosarcoma and encourage further research.
Identifiants
pubmed: 35820864
doi: 10.1186/s12885-022-09857-x
pii: 10.1186/s12885-022-09857-x
pmc: PMC9275282
doi:
Substances chimiques
Naphthoquinones
0
Receptors, Death Domain
0
shikonin
3IK6592UBW
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
758Informations de copyright
© 2022. The Author(s).
Références
Endocr Connect. 2017 Feb;6(2):53-62
pubmed: 28069896
Toxicol Pathol. 2007 Jun;35(4):495-516
pubmed: 17562483
BMC Cancer. 2019 Jan 7;19(1):20
pubmed: 30616572
Bioorg Med Chem Lett. 2022 Feb 1;57:128503
pubmed: 34922028
J Nat Prod. 2020 Feb 28;83(2):305-315
pubmed: 31961147
Int J Cancer. 2015 Sep 15;137(6):1446-56
pubmed: 25688715
Mol Cancer Ther. 2004 Feb;3(2):187-97
pubmed: 14985459
Front Pharmacol. 2020 May 27;11:748
pubmed: 32536866
Bone Joint J. 2019 Mar;101-B(3):266-271
pubmed: 30813783
J Cancer. 2022 Jan 1;13(1):243-252
pubmed: 34976186
Int J Mol Sci. 2022 Mar 21;23(6):
pubmed: 35328817
Nat Rev Cancer. 2010 Jul;10(7):481-8
pubmed: 20535132
Biochem J. 2010 Sep 1;430(2):199-205
pubmed: 20704571
Biochem Pharmacol. 2014 Apr 1;88(3):322-33
pubmed: 24522113
Oncogenesis. 2016 May 09;5:e222
pubmed: 27159675
Sci Rep. 2018 Feb 20;8(1):3317
pubmed: 29463831
Cancers (Basel). 2022 Feb 22;14(5):
pubmed: 35267423
Methods Mol Biol. 2014;1170:29-40
pubmed: 24906307
Pharmacol Res. 2019 Nov;149:104463
pubmed: 31553936
BMC Cell Biol. 2018 Dec 29;19(1):29
pubmed: 30594131
Pancreatology. 2021 Apr;21(3):630-641
pubmed: 33707115
IUBMB Life. 2006 Nov;58(11):621-31
pubmed: 17085381
Cell Transplant. 2021 Jan-Dec;30:963689720979162
pubmed: 33508949
Pharm Biol. 2020 Dec;58(1):950-958
pubmed: 32956595
Anal Cell Pathol (Amst). 2021 Nov 6;2021:6435393
pubmed: 34782853
Int J Mol Sci. 2021 Mar 09;22(5):
pubmed: 33803437
Life Sci. 2018 Jul 1;204:71-77
pubmed: 29738778
In Vivo. 2008 May-Jun;22(3):305-9
pubmed: 18610740
J Nat Prod. 2012 May 25;75(5):865-9
pubmed: 22530779
Mol Med Rep. 2021 Aug;24(2):
pubmed: 34109434
Biomed Res Int. 2014;2014:150845
pubmed: 25013758
Cancers (Basel). 2021 May 14;13(10):
pubmed: 34069269
Mol Med Rep. 2017 Sep;16(3):3055-3060
pubmed: 28713949
Biosci Rep. 2021 Jan 29;41(1):
pubmed: 33403388
Eur J Biochem. 1998 Jun 15;254(3):439-59
pubmed: 9688254
Cancer Causes Control. 2015 Aug;26(8):1127-39
pubmed: 26054913
Oncology. 2005;69 Suppl 3:4-10
pubmed: 16301830
Crit Rev Oncol Hematol. 2019 May;137:57-83
pubmed: 31014516
FASEB J. 1995 Jun;9(9):726-35
pubmed: 7601337
Radiat Oncol. 2019 Nov 21;14(1):206
pubmed: 31752953
J Ethnopharmacol. 2010 May 27;129(2):182-8
pubmed: 20226848