Anthricininduced caspasedependent apoptosis through IGF1R/PI3K/AKT pathway inhibition in A549 human nonsmall lung cancer cells.
Oncol Rep
; 39(6): 2769-2776, 2018 Jun.
Article
in En
| MEDLINE
| ID: mdl-29620219
ABSTRACT
Anthricin (deoxypodophyllotoxin) is a major lignan in Anthriscus sylvestris and possesses many bioactivities such as antiproliferative, antitumor, antiplatelet aggregation, antiviral and antiinflammatory actions. However, the anticancer effects of anthricin on A549 human nonsmall cell lung cancer cells and potential molecular mechanisms remain unknown. Therefore, we investigated the anticancer effect of anthricin and the underlying mechanism in A549 cells. Anthricin (10200 nM) inhibited the viability of A549 cells in a dose and timedependent manner. Moreover, anthricininduced apoptosis was confirmed by live and dead assay, 4,6dianmidino2phenylindole staining, and flow cytometric analysis. In addition, anthricin induced cell cycle arrest at the G2/M phase through suppression of the expression of cell cycle cascade proteins, Cdc2 and Cdc25C. Furthermore, it induced the expression of caspaserelated proteins and significantly suppressed the phosphorylation of insulinlike growth factor 1 receptor (IGF1R), PI3K and Akt. Anthricin significantly inhibited tumor growth without any significant change in the body weight of mice in A549 tumor xenograft BALB/c nude mice. Anthricin induced caspasedependent apoptosis through the IGF1R/PI3K/Akt signaling pathway in A549 cells.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Signal Transduction
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Carcinoma, Non-Small-Cell Lung
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Caspases
/
Heterocyclic Compounds, 4 or More Rings
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Lung Neoplasms
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Antineoplastic Agents
Type of study:
Prognostic_studies
Limits:
Animals
/
Humans
Language:
En
Journal:
Oncol Rep
Journal subject:
NEOPLASIAS
Year:
2018
Document type:
Article