Critical roles of mucin-1 in sensitivity of lung cancer cells to tumor necrosis factor-alpha and dexamethasone
Lung cancer is the leading cause of death from cancer. Mucins are glycoproteins with high molecular weight, responsible for cell growth, differentiation, and signaling, and were proposed to be correlated with gene heterogeneity of lung cancer. Here, we report aberrant expression of mucin genes and tumor necrosis factor receptors in lung adenocarcinoma tissues compared with normal tissues in GEO datasets. Mucin-1 (MUC1) gene was selected and considered as the target gene; furthermore, the expression pattern of adenocarcinomic cells (A549, H1650, or H1299 cells) was validated under the stimulation with tumor necrosis factor-alpha (TNFα) or dexamethasone (DEX), separately. MUC1 gene interference was done to A549 cells to show its role in sensitivity of lung cancer cells to TNFα and DEX. Results of our experiments indicate that MUC1 may regulate the influence of inflammatory mediators in effects of glucocorticoids (GCs), as a regulatory target to improve therapeutics. It shows the potential effect of MUC1 and GCs in lung adenocarcinoma (LADC), which may help in LADC treatment in the future.
KeywordsLung cancer Mucin-1 Tumor necrosis factor-alpha Dexamethasone Therapeutics
The work was supported by Shanghai Leading Academic Discipline Project (B115), Zhongshan Distinguished Professor Grant (XDW), The National Nature Science Foundation of China (91230204, 81270099, 81320108001, 81270131, 81400035, 81570075, 81500058, 81500025), The Shanghai Committee of Science and Technology (12JC1402200, 12431900207, 11410708600), Zhejiang Provincial Natural Science Foundation (Z15H010002), and Zhejiang Provincial Science Technology Department Foundation (WKJ-ZJ-1526).
Compliance with ethical standards
All experimental procedures were approved by the Zhongshan Hospital Research Ethics Committee, Fudan University, China.
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