Cystic fibrosis and the relationship between mucin and chloride secretion by cultures of human airway gland mucous cells.

We investigated how cystic fibrosis (CF) alters the relationship between Cl(-) and mucin secretion in cultures of non-CF and CF human tracheobronchial gland mucous (HTGM and CFTGM, respectively) cells. Biochemical studies showed that HTMG cells secreted typical airway mucins, and immunohistochemical studies showed that these cells expressed MUC1, MUC4, MUC5B, MUC8, MUC13, MUC16, and MUC20. Effects of cumulative doses of methacholine (MCh), phenylephrine (Phe), isoproterenol (Iso), and ATP on mucin and Cl(-) secretion were studied on HTGM and CFTGM cultures.

Wnt and Hedgehog are critical mediators of cigarette smoke-induced lung cancer.

Background: Lung cancer is the leading cause of cancer death in the world, and greater than 90% of lung cancers are cigarette smoke-related. Current treatment options are inadequate, because the molecular basis of cigarette-induced lung cancer is poorly understood.

Methodology/principal Findings: Here, we show that human primary or immortalized bronchial epithelial cells exposed to cigarette smoke for eight days in culture rapidly proliferate, show anchorage-independent growth, and form tumors in nude mice.

Tobacco smoke control of mucin production in lung cells requires oxygen radicals AP-1 and JNK.

In smokers' lungs, excessive mucus clogs small airways, impairing respiration and promoting recurrent infection. A breakthrough in understanding this pathology was the realization that smoke could directly stimulate mucin synthesis in lung epithelial cells and that this phenomenon was dependent on the cell surface receptor for epidermal growth factor, EGFR. Distal steps in the smoke-triggered pathway have not yet been determined.

DNA methylation regulates the expression of Y chromosome specific genes in prostate cancer.

Purpose: We hypothesized that DNA methylation regulates the differential expression of Y chromosome specific genes in prostate cancer. To test this hypothesis we analyzed the expression of Y chromosome specific genes in 5-aza-2'-deoxycytidine (5-azaC) treated and untreated prostate cancer cell lines.

Materials And Methods: To test this hypothesis Y chromosome specific genes were analyzed in prostate cancer cells treated with the demethylation agent 5-azaC.