Naphthalene allyl trifluoromethyl benzocyclopentanone inhibits proliferation and induces apoptosis of lung cancer A549 cells in vitro.
10.12122/j.issn.1673-4254.2022.02.05
- Author:
Xu WU
1
;
Jun Jie HE
1
;
Ping LI
1
;
Yi WANG
2
;
Liang YAN
1
;
Jin Zhu MA
1
Author Information
1. Anhui Key Laboratory of Active Biomacromolecules, Wannan Medical College, Wuhu 241002, China.
2. School of Chemistry and Chemical Engineering, Nanjing University, Nanjing 210000, China.
- Publication Type:Journal Article
- Keywords:
Akt/mTOR signal pathway;
apoptosis;
cell cycle;
cell proliferation;
naphthalene allyl trifluoromethyl benzocyclopentanone
- MeSH:
A549 Cells;
Animals;
Apoptosis;
Cell Proliferation;
Humans;
Lung Neoplasms/metabolism*;
Mice;
Naphthalenes/pharmacology*
- From:
Journal of Southern Medical University
2022;42(2):201-206
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the molecular mechanism by which a novel naphthalene allyl trifluoromethyl benzocyclopentanone XX0335 inhibits the proliferation and induces apoptosis of lung cancer A549 cells.
METHODS:Lung cancer A549 cells were treated with 0.1% DMSO (control) or different concentrations (6.25, 12.5, and 25 μg/mL) of XX0335, and the changes in cell viability, cell cycle, proliferation and apoptosis were assessed with CCK-8 assay, EdU experiment, and flow cytometry. The effects of different concentrations of XX0335 on phosphorylation levels of proliferation-related proteins Akt, mTOR, Akt/mTOR and the expressions of cleaved PARP and cyclin D1 were determined using Western blotting. We also assessed the effect of XX0335 on tumor growth in a mouse model bearing A945 cell xenograft.
RESULTS:Treatment with XX0335 reduced the viability of A549 cells in a dose-dependent manner (P < 0.01) and significantly inhibited cell proliferation (P < 0.001). Flow cytometry showed that XX0335 treatment promoted apoptosis of the cells (P < 0.01) and caused an obvious increase of the number of G1-phase cells. Compared with DMSO, XX0335 significantly inhibited the phosphorylation of Akt and mTOR, increased the expression of cleaved PARP, and lowered the protein expression of cyclin D1. In the tumor-bearing mouse models, injection of XX0335 significantly decreased the tumor volume (P < 0.01).
CONCLUSION:XX0335 inhibits the proliferation, cycle and induces apoptosis of lung cancer A549 cells possibly by inhibiting the Akt/mTOR signal pathway.
