Eriocalyxin B induces apoptosis in human triple negative breast cancer cells via inhibiting STAT3 activation and mitochondrial dysfunction.
Antineoplastic Agents, Phytogenic
/ pharmacology
Apoptosis
/ drug effects
Caspase 3
/ metabolism
Cell Line, Tumor
Cell Proliferation
/ drug effects
Diterpenes
/ pharmacology
Female
Humans
MCF-7 Cells
Mitochondria
/ drug effects
Mitochondrial Diseases
/ drug therapy
NF-kappa B
/ metabolism
Proto-Oncogene Proteins c-bcl-2
/ metabolism
STAT3 Transcription Factor
/ antagonists & inhibitors
Signal Transduction
/ drug effects
Triple Negative Breast Neoplasms
/ drug therapy
Journal
Pakistan journal of pharmaceutical sciences
ISSN: 1011-601X
Titre abrégé: Pak J Pharm Sci
Pays: Pakistan
ID NLM: 9426356
Informations de publication
Date de publication:
Nov 2019
Nov 2019
Historique:
entrez:
7
2
2020
pubmed:
7
2
2020
medline:
2
7
2020
Statut:
ppublish
Résumé
Eriocalyxin B (EriB), a potent ent-kaurene extracted from Isodon eriocalyx, has turned up as novel anti-cancer agent during recent years against a range of cancer types. TNBC (Triple negative breast cancer) is highly aggressive breast cancer, which is resistant towards current therapeutics due to absence of drug targets. Here, we have probed the molecular mechanism of EriB-induced apoptosis in TNBC (MDA-MB231) cells to check whether its anticancer activity is mediated by modulation of STAT3 and NF-ϰB. EriB induced apoptosis in MDA-MB231 cells via inhibiting NF-ϰBp65, STAT3 phosphorylation, increasing Bax/Bcl-2 ratio, MMP dissipation, and activation of caspase-3. These results provide a rationale for further in vivo investigations on EriB, which might also prove to be a potential drug candidate for developing novel therapeutics against TNBC.
Substances chimiques
Antineoplastic Agents, Phytogenic
0
Diterpenes
0
NF-kappa B
0
Proto-Oncogene Proteins c-bcl-2
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
eriocalyxin B
0
Caspase 3
EC 3.4.22.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM