Aquaporin 5 expression increases mucin production in lung adenocarcinoma.
نویسندگان
چکیده
Our recent studies have demonstrated that AQP5 is involved in the metastatic potential of lung cancer. Here, our aim was to explore the effects of AQP5 expression on mucin production in lung adenocarcinoma. We tested MUC5AC and MUC5B mucin production induced by AQP5 expression in lung adenocarcinoma metastasis. Lung adenocarcinoma cells with different levels of AQP5 expression were used in this study. In another set of experiments, deletion of AQP5 was studied using AQP5 (-/-) mice. Significantly increased expression of MUC5AC and MUC5B mucin was found in AQP5 high-expressing tumor cells, which suggested that mucin production induced by AQP5 may contribute to the enhanced metastatic potential in lung adenocarcinoma cells. Our results also showed that AQP5 expression increases MUC5AC and MUC5B mucin production and that this may be partly through the EGFR signaling pathway. In brief, our results provide evidence that mucin production induced by AQP5 expression may play important roles in enhanced metastasis potential in lung adenocarcinoma.
منابع مشابه
Aquaporin 5 Expression and Its Relationship to Apoptosis in Different Grades of Differentiated Non-Small Cell Lung Carcinoma
Aquaporin 5 has been recently found as an important oncogenic marker whose expression levels seem to be determined by the level of cellular differentiation. Despite aquaporin volume decrease (AVD) being the most conserved earliest event in apoptosis, there is still a paucity of studies exploring on aquaporin expression and its relationship with apoptosis in cancer. The aim of this study was to ...
متن کاملCharacterization of air-liquid interface culture of A549 alveolar epithelial cells
Alveolar epithelia play an essential role in maintaining the integrity and homeostasis of lungs, in which alveolar epithelial type II cells (AECII) are a cell type with stem cell potential for epithelial injury repair and regeneration. However, mechanisms behind the physiological and pathological roles of alveolar epithelia in human lungs remain largely unknown, partially owing to the difficult...
متن کاملTherapeutic Discovery Targeting the Intracellular MUC1 C-terminal Domain Inhibits Proliferation and Estrogen Receptor Transcriptional Activity in Lung Adenocarcinoma Cells
Mucin 1 (MUC1) is a diagnostic factor and therapy target in lung adenocarcinoma. MUC1 C-terminal intracellular domain (CD) interacts with estrogen receptor (ER) a and increases gene transcription in breast cancer cells. Because lung adenocarcinoma cells express functional ERa and ERb, we examined MUC1 expression and MUC1–ER interaction. Because blocking MUC1 CD with an inhibitory peptide (PMIP)...
متن کاملTargeting the intracellular MUC1 C-terminal domain inhibits proliferation and estrogen receptor transcriptional activity in lung adenocarcinoma cells.
Mucin 1 (MUC1) is a diagnostic factor and therapy target in lung adenocarcinoma. MUC1 C-terminal intracellular domain (CD) interacts with estrogen receptor (ER) α and increases gene transcription in breast cancer cells. Because lung adenocarcinoma cells express functional ERα and ERβ, we examined MUC1 expression and MUC1-ER interaction. Because blocking MUC1 CD with an inhibitory peptide (PMIP)...
متن کاملEffects of dexamethasone on Muc5ac mucin production by primary airway goblet cells.
Mucus hypersecretion associated with airway inflammation is reduced by glucocorticoids. Two mechanisms of glucocorticoid-mediated inhibition of mucus production have been proposed, direct inhibition of mucus production by airway epithelial cells and indirectly through inhibition of proinflammatory mediators that stimulate mucus production. In this study, we examined the effect of dexamethasone ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Oncology reports
دوره 25 6 شماره
صفحات -
تاریخ انتشار 2011