α5-nAChR modulates nicotine-induced cell migration and invasion in A549 lung cancer cells

2015 ◽  
Vol 67 (9) ◽  
pp. 477-482 ◽  
Author(s):  
Haiji Sun ◽  
Xiaoli Ma
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
A549 Lung

scholarly journals Propolin C Inhibited Migration and Invasion via Suppression of EGFR-Mediated Epithelial-to-Mesenchymal Transition in Human Lung Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-15
Author(s):  
Jih-Tung Pai ◽  
Yi-Chin Lee ◽  
Si-Ying Chen ◽  
Yann-Lii Leu ◽  
Meng-Shih Weng
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial To Mesenchymal Transition ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion

Controlling lung cancer cell migration and invasion via epithelial-to-mesenchymal transition (EMT) through the regulation of epidermal growth factor receptor (EGFR) signaling pathway has been demonstrated. Searching biological active phytochemicals to repress EGFR-regulated EMT might prevent lung cancer progression. Propolis has been used as folk medicine in many countries and possesses anti-inflammatory, antioxidant, and anticancer activities. In this study, the antimigration and anti-invasion activities of propolin C, a c-prenylflavanone from Taiwanese propolis, were investigated on EGFR-regulated EMT signaling pathway. Cell migration and invasion activities were dose-dependently suppressed by noncytotoxic concentration of propolin C. Downregulations of vimentin and snail as well as upregulation of E-cadherin expressions were through the inhibition of EGFR-mediated phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and extracellular signal-regulated kinase (ERK) signaling pathway in propolin C-treated cells. In addition, EGF-induced migration and invasion were suppressed by propolin C-treated A549 lung cancer cells. No significant differences in E-cadherin expression were observed in EGF-stimulated cells. Interestingly, EGF-induced expressions of vimentin, snail, and slug were suppressed through the inhibition of PI3K/Akt and ERK signaling pathway in propolin C-treated cells. Inhibition of cell migration and invasion by propolin C was through the inhibition of EGF/EGFR-mediated signaling pathway, followed by EMT suppression in lung cancer.

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.

Downregulation of microRNA-3646 Through Direct Targeting of F-Box Protein 4 on Interleukin-17-Induced Lung Cancer Cell Migration and Invasion

2021 ◽  
Vol 11 (7) ◽  
pp. 1429-1434
Author(s):  
Ling Lin ◽  
Hongjie Zhao ◽  
Liqiang Zhai ◽  
Baoxin Xu ◽  
Ling Xiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Carcinoma ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Aberrant Expression ◽  
And Migration ◽  
E Cadherin

IL-17 participates in the initiation and growth of malignant cancers, including lung cancer. The aberrant expression of miRNA is also related to tumor growth and metastasis. Studies have confirmed that high expression of miRNA-3646 can boost breast cancer cell invasion and migration, suggesting that miRNA-3646 is a tumor-promoting factor. However, the role of miRNA-3646 in the migration and invasion of IL-17-induced lung cancer cells is unclear. In this study, qRT-PCR was used to determine the level of miRNA-3646. We found that in lung cancer cells, miRNA-3646 levels exceeded those of normal bronchial epithelial 16HBE cells (P < 0.05). The level of miRNA-3646 in NCI-H1299 cells was higher than that in A549, NCI-H446, and SK-MES-1 cells (P < 0.05). After IL-17 treatment, the number of proliferating and migrating lung carcinoma NCI-H1299 cells increased, transport of vimentin increased, and transport of E-cadherin decreased (P < 0.05). After IL-17 treatment, the number of proliferating and migrating lung carcinoma NCI-H1299 cells transfected with miRNA-3646 inhibitor decreased, transport of vimentin decreased, and transport of E-cadherin increased (P < 0.05). FBXO4 siRNA reversed the inhibition of miRNA-3646 on the proliferation and migration of IL-17-induced lung carcinoma NCI-H1299 cells and the transport of E-cadherin and vimentin. Thus, downregulation of miRNA-3646 inhibited IL-17-induced lung carcinoma cell migration and proliferation by directly targeting FBXO4.

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
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