scholarly journals TIMP-2 modulates cancer cell transcriptional profile and enhances E-cadherin/beta-catenin complex expression in A549 lung cancer cells

Oncotarget ◽  
2013 ◽  
Vol 4 (1) ◽  
pp. 163-173 ◽  
Author(s):  
Dimitra Bourboulia ◽  
HuiYing Han ◽  
Sandra Jensen-Taubman ◽  
Noah Gavil ◽  
Biju Isaac ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Transcriptional Profile ◽  
Lung Cancer Cells ◽  
Beta Catenin ◽  
A549 Lung ◽  
Complex Expression ◽  
E Cadherin

Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways

MedChemComm ◽  
2016 ◽  
Vol 7 (6) ◽  
pp. 1197-1203 ◽  
Author(s):  
Ravindra M. Kumbhare ◽  
Tulshiram L. Dadmal ◽  
Dinesh Kumar ◽  
M. Janaki Ramaiah ◽  
Anudeep Kota ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Signalling Pathways ◽  
Lung Cancer Cell ◽  
Cancer Cell Death ◽  
A549 Lung Cancer Cell ◽  
A549 Lung

Fluorinated thiazolidinols cause A549 lung cancer cell death by acting via PI3K/Akt/mTOR and MEK/ERK pathways.

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.

A synthesized butyrolactone derivative in combination with chloroquine can inhibit cancer cell growth and lysosome vacuolation induced by chloroquine in A549 lung cancer cells

RSC Advances ◽  
2016 ◽  
Vol 6 (59) ◽  
pp. 54099-54101
Author(s):  
Xin-Peng Chen ◽  
Chuan-Dong Fan ◽  
Le Su ◽  
Bao-Xiang Zhao ◽  
Jun-Ying Miao
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Atpase Activity ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
A549 Lung

3BDO in combination with chloroquine could elevate the Na+,K+-ATPase activity and decrease the expression of competing endogenous non-coding RNA TGFB2-OT1. Therefore, ​ the combination inhibited the cells growth and lysosomal vacuolation induced by CQ.

scholarly journals Proteasome Inhibitor Immunotherapy for the Epithelial to Mesenchymal Transition: Assessing the A549 Lung Cancer Cell Microenvironment and the Role of M1, M2a and M2c ‘Hydrocortisone-Polarised’ Macrophages

2022 ◽  
Author(s):  
Selin Engür Öztürk ◽  
Miriş DİKMEN
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
A549 Cell ◽  
Epithelial To Mesenchymal Transition ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Mesenchymal Transition ◽  
Cell Microenvironment ◽  
A549 Lung

Abstract Lung cancer is a leading cause of cancer-related deaths, primarily as a result of metastases. In this metastasis, the epithelial-to-mesenchymal transition (EMT) is essential. Interaction with the cancer cell microenvironment is primarily dependent on M1- and M2-polarized macrophage. In this study, we revealed the EMT-associated activity of M1, M2a and M2c macrophages in A549 lung cancer cells. We established a co-culture model of A549 lung cancer cells utilizing THP-1-derived M1/M2 polarised macrophages to explore the involvement of macrophages in the immune response, apoptosis, and EMT in lung cancer. Although multiple polarising agents are routinely used for M1 and M2 conversion, we assessed a new possible polarising agent, hydrocortisone. M1 increased A549 cell sensitivity to proteasome inhibitors and decreased A549 cell viability by inducing apoptosis. EMT was induced in the presence of M2c macrophages in A549 cells by the levels of vimentin, fibronectin, E-cadherin, NF-kB, CCL-17. We also revealed the antiproliferative effects of bortezomib and ixazomib on A549 cells in both 2D and 3D cultures. Our findings could help develop an immunotherapeutic strategy by shedding light on a previously undiscovered part of the EMT pathway. Furthermore, additional investigation may reveal that polarising tumour-associated macrophages to M1 and eliminating the M2a or particularly the M2c subtype are effective anti-cancer strategies.

Discovery of 2′-hydroxychalcones as autophagy inducer in A549 lung cancer cells

2014 ◽  
Vol 12 (19) ◽  
pp. 3062-3070 ◽  
Author(s):  
Fang-Wu Wang ◽  
Sheng-Qing Wang ◽  
Bao-Xiang Zhao ◽  
Jun-Ying Miao
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Lung Cancer Cell ◽  
A549 Lung Cancer Cell ◽  
A549 Lung

A series of 2′-hydroxychalcone derivatives was synthesized and the effects of all the compounds on growth of A549 lung cancer cell were investigated.

scholarly journals TLE1 promotes EMT in A549 lung cancer cells through suppression of E-cadherin

2014 ◽  
Vol 455 (3-4) ◽  
pp. 277-284 ◽  
Author(s):  
Xin Yao ◽  
Shubha Kale Ireland ◽  
Tri Pham ◽  
Brandi Temple ◽  
Renwei Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
A549 Lung ◽  
E Cadherin
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