2013年9月18日訊 /生物谷BIOON/--近期發布在Journal of Cellular Biochemistry上的文章稱，產生粘液的"惡性循環"能夠保護子宮和胰腺癌細胞，促進其癌細胞增殖。該研究為治療癌症提供了新的方向。
液能夠附著於諸如肺、胃，腸道等內臟器官上皮細胞表明，保護器官不受細菌侵染。但是滑膩膩的粘液也能讓癌細胞更為猖獗，粘液完全附著在癌細胞的表明，幫助其轉移，保護癌細胞免受化療藥物和免疫系統的攻擊。
該研究發現形成粘液的糖蛋白MUC1過表達不僅能夠保護癌細胞還能夠促進癌細胞轉移，由於細胞的反饋循環使得表皮生長因子（EGFP）和MUC1相互促進形成惡性循環。
EGFR是一種跨膜蛋白，該蛋白能夠刺激正常細胞生長，分裂和分化。該文章的通訊作者Carson博士稱，之前從沒有人考慮過刺激EGFR能夠激活MUC1的表達，而MUC1又能進一步增加EGFR的水平，形成一個惡性循環。
Carson博士稱，粘液覆蓋於癌細胞表面，使得免疫細胞和化療藥物不能接觸到癌細胞，從而不能產生殺傷的效果。
一種備受爭議的治療糖尿病的藥物rosiglitazone（羅格列酮）有望緩解該惡性循環，rosiglitazone被認為長期使用會引起糖尿病病人產生心臟方面問題。但是在培養細胞中檢測rosiglitazone的效果，科學家發現概要能夠有效的抑制EGFR的激活，降低MUC1的表達。
Carson博士稱證明rosiglitazone藥物的效果還需要更多的實驗，我們希望能夠通過修飾該藥物降低其副作用，增加藥效。（生物谷Bioon.com）
Activated EGFR stimulates MUC1 expression in human uterine and pancreatic cancer cell lines
Neeraja Dharmaraj, Brian J. Engel, Daniel D. Carson
MUC1 is a large cell surface mucin glycoprotein that plays diverse roles in both normal and tumor cell biology. These roles include mucosal hydration and protection, inhibition of embryo implantation, protection of tumor cells from the immune system and reduction of cytotoxic drug uptake. Similarly, the EGFR family of cell surface receptors drives many normal developmental processes as well as various aspects of tumor growth and gene expression. EGFR family members have been demonstrated to form complexes with MUC1 in various cellular contexts. Nonetheless, the role that EGFR activation plays in modulating MUC1 levels has not been considered. In this study, we demonstrate that activated EGFR drives high level MUC1 expression in multiple cell lines of uterine adenocarcinoma and pancreatic cancer origins. In some cells, addition of exogenous EGFR ligands (EGF or HB-EGF) elevates MUC1 levels while addition of the EGFR tyrosine kinase inhibitor, AG1478, reduces MUC1 levels. The thiazolidinedione, rosiglitazone, previously shown to reduce progesterone-stimulated MUC1 expression, also blocks EGFR ligand-driven MUC1 expression. This activity was observed at relatively high rosiglitazone concentrations (above 10?μM) and appeared to be largely PPARγ independent indicating a novel utility of this drug to reduce mucin-expression in various tumor settings. Collectively, these data demonstrate that: (1) activation of EGFR stimulates MUC1 expression in multiple cellular contexts and (2) it may be possible to develop useful interventions to reduce MUC1 expression as a complementary strategy for tumor therapy