Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/94087
標題: Digoxin Suppresses Tumor Malignancy through Inhibiting Multiple Src-Related Signaling Pathways in Non-Small Cell Lung Cancer
作者: Lin, Sheng-Yi
Chang, Hsiu-Hui
Lai, Yi-Hua
Lin, Ching-Hsiung
Chen, Min-Hsuan
Chang, Gee-Chen
Tsai, Meng-Feng
Chen, Jeremy J W
關鍵字: Antineoplastic Agents
Carcinoma, Non-Small-Cell Lung
Cell Death
Cell Line, Tumor
Cell Movement
Cell Survival
Digoxin
Enzyme Activation
Focal Adhesion Protein-Tyrosine Kinases
Gene Expression Regulation, Neoplastic
Humans
Lung Neoplasms
Models, Biological
Neoplasm Invasiveness
Phosphorylation
RNA, Messenger
Receptor, Epidermal Growth Factor
STAT3 Transcription Factor
Tumor Stem Cell Assay
src-Family Kinases
Signal Transduction
摘要: Non-small cell lung cancer is the predominant type of lung cancer, resulting in high mortality worldwide. Digoxin, a cardiac glycoside, has recently been suggested to be a novel chemotherapeutic agent. Src is an oncogene that plays an important role in cancer progression and is therefore a potential target for cancer therapy. Here, we investigated whether digoxin could suppress lung cancer progression through the inhibition of Src activity. The effects of digoxin on lung cancer cell functions were investigated using colony formation, migration and invasion assays. Western blotting and qPCR assays were used to analyze the mRNA and protein expression levels of Src and its downstream proteins, and a cell viability assay was used to measure cellular cytotoxicity effects. The results of the cell function assays revealed that digoxin inhibited the proliferation, invasion, migration, and colony formation of A549 lung cancer cells. Similar effects of digoxin were also observed in other lung cancer cell lines. Furthermore, we found that digoxin significantly suppressed Src activity and its protein expression in a dose- and time-dependent manner as well as reduced EGFR and STAT3 activity. Our data suggest that digoxin is a potential anticancer agent that may suppress lung cancer progression through inhibiting Src and the activity of related proteins.
URI: http://hdl.handle.net/11455/94087
Appears in Collections:生物科技發展中心

文件中的檔案:

取得全文請前往華藝線上圖書館



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.