scholarly journals Progesterone inhibits the migration and invasion of A549 lung cancer cells through membrane progesterone receptor α-mediated mechanisms

2013 ◽  
Vol 29 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
MINGXUAN XIE ◽  
SHAOJIN YOU ◽  
QIONG CHEN ◽  
XI CHEN ◽  
CHENGPING HU
Keyword(s):  
Lung Cancer ◽  
Progesterone Receptor ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Membrane Progesterone Receptor ◽  
A549 Lung

Paris Saponin VII Inhibits the Migration and Invasion in Human A549 Lung Cancer Cells

2015 ◽  
Vol 29 (9) ◽  
pp. 1366-1372 ◽  
Author(s):  
Lei Fan ◽  
Yuhua Li ◽  
Yang Sun ◽  
Jing Han ◽  
Zhenggang Yue ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Human A549 ◽  
A549 Lung

Peniciketal A, A Novel Spiroketal Compound, Exerts Anticancer Effects by Inhibiting Cell Proliferation, Migration and Invasion of A549 Lung Cancer Cells

2019 ◽  
Vol 18 (11) ◽  
pp. 1573-1581 ◽  
Author(s):  
Xue Gao ◽  
Yuming Zhou ◽  
Xiaoqi Zheng ◽  
Hongliu Sun ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Normal Fibroblast ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Anticancer Effects ◽  
A549 Lung

Background: Peniciketal A (Pe-A) is a spiroketal compound isolated from saline soil-derived fungus Penicillium raistrickii. However, its role for biological processes has not been clarified. In this study, we for the first time investigated the anticancer effects and the underlying mechanisms of Pe-A in A549 lung cancer cells. Metheds: Cell proliferation was tested by MTT assay and colony formation assay. Flow cytometry was performed to examine the cell cycle, apoptosis and mitochondrial membrane potential. Invasion and migration were analyzed using transwell assay and wound healing analysis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. Results: Pe-A effectively inhibited proliferation, with IC50 values was 22.33 μM for 72 h. Mechanistic studies revealed that Pe-A caused cell cycle arrest at the G0-G1 phase by decreasing cyclinD1 expression and induced apoptosis through accelerating the mitochondrial apoptotic pathway. Moreover, Pe-A significantly inhibited A549 cell migration and invasion by reducing the protein levels of MMP-2 and MMP-9, while the Epithelial- Mesenchymal Transition (EMT) property was also changed. Importantly, Pe-A exhibited much lower toxicity towards L02, normal liver cells, and MRC5, normal fibroblast cells, compared to A549 cells. Conclusion: Collectively, the current results indicate that Pe-A may offer effective potentials and insights for lung cancer treatment and drug design.

scholarly journals Ovalitenone Inhibits the Migration of Lung Cancer Cells via the Suppression of AKT/mTOR and Epithelial-to-Mesenchymal Transition

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 638
Author(s):  
Kittipong Sanookpan ◽  
Nongyao Nonpanya ◽  
Boonchoo Sritularak ◽  
Pithi Chanvorachote
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Colony Formation ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Cancer metastasis is the major cause of about 90% of cancer deaths. As epithelial-to-mesenchymal transition (EMT) is known for potentiating metastasis, this study aimed to elucidate the effect of ovalitenone on the suppression of EMT and metastasis-related behaviors, including cell movement and growth under detached conditions, and cancer stem cells (CSCs), of lung cancer cells. Methods: Cell viability and cell proliferation were determined by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazo-liumbromide (MTT) and colony formation assays. Cell migration and invasion were analyzed using a wound-healing assay and Boyden chamber assay, respectively. Anchorage-independent cell growth was determined. Cell protrusions (filopodia) were detected by phalloidin-rhodamine staining. Cancer stem cell phenotypes were assessed by spheroid formation. The proteins involved in cell migration and EMT were evaluated by Western blot analysis and immunofluorescence staining. Results: Ovalitenone was used at concentrations of 0–200 μM. While it caused no cytotoxic effects on lung cancer H460 and A549 cells, ovalitenone significantly suppressed anchorage-independent growth, CSC-like phenotypes, colony formation, and the ability of the cancer to migrate and invade cells. The anti-migration activity was confirmed by the reduction of filopodia in the cells treated with ovalitenone. Interestingly, we found that ovalitenone could significantly decrease the levels of N-cadherin, snail, and slug, while it increased E-cadherin, indicating EMT suppression. Additionally, the regulatory signaling of focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), the mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) was suppressed by ovalitenone. Conclusions: The results suggest that ovalitenone suppresses EMT via suppression of the AKT/mTOR signaling pathway. In addition, ovalitenone exhibited potential for the suppression of CSC phenotypes. These data reveal the anti-metastasis potential of the compound and support the development of ovalitenone treatment for lung cancer therapy.

Sign in / Sign up

Export Citation Format

Share Document