Foeniculum vulgare seed extract induces apoptosis in lung cancer cells partly through the down-regulation of Bcl-2.
Animals
Antineoplastic Agents, Phytogenic
/ isolation & purification
Apoptosis
/ drug effects
Cell Line, Tumor
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Foeniculum
/ chemistry
Gene Expression Regulation, Neoplastic
Humans
Lung Neoplasms
/ drug therapy
Male
Mice, Inbred BALB C
Mice, Nude
Plant Extracts
/ isolation & purification
Proto-Oncogene Proteins c-bcl-2
/ genetics
Seeds
Signal Transduction
Tumor Burden
/ drug effects
Xenograft Model Antitumor Assays
Apoptosis
Bcl-2
Chemotherapy
Foeniculum vulgare
Lung cancer
Journal
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295
Informations de publication
Date de publication:
Mar 2021
Mar 2021
Historique:
received:
12
04
2020
revised:
07
12
2020
accepted:
26
12
2020
pubmed:
5
1
2021
medline:
20
7
2021
entrez:
4
1
2021
Statut:
ppublish
Résumé
The factors behind the pathogenesis of lung cancer are not clear, and treatment failure is generally caused by drug resistance, recurrence, and metastasis. Development of new therapeutic agents to overcome drug-resistance remains a challenge clinically. Various extracts of Foeniculum vulgare have shown promising anticancer activity; however, effects on lung cancer and the underlying molecular mechanisms of action are not clear. In the present study, we found that the ethanol extract of Foeniculum vulgare seeds (EEFS) significantly reduced lung cancer cell growth in vitro and in vivo. EEFS decreased the viability of and triggered apoptosis in the lung cancer cell lines NCI-H446 and NCI-H661. EEFS induced apoptosis mainly through inhibition of Bcl-2 protein expression, reduction of mitochondrial membrane potential, and release of Cytochrome C. Moreover, EEFS significantly inhibited colony formation and cell migration in lung cancer cells. EEFS also effectively inhibited the growth of xenograft tumors derived from NCI-446 cells by reducing Bcl-2 protein expression and inducing apoptosis. Taken together, these findings suggest that EEFS exerts anti-lung cancer activity by targeting the Bcl-2 protein and may have potential as a therapeutic drug for lung cancer.
Identifiants
pubmed: 33395604
pii: S0753-3322(20)31406-2
doi: 10.1016/j.biopha.2020.111213
pii:
doi:
Substances chimiques
Antineoplastic Agents, Phytogenic
0
BCL2 protein, human
0
Plant Extracts
0
Proto-Oncogene Proteins c-bcl-2
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
111213Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.