There is a critical balance between proliferation, differ entiati

There is a critical balance between proliferation, differ entiation, and apoptosis in the cellular composition of every tissue. In the hematopoietic system, MYB clearly plays a role in maintaining this balance. MYB is essential for hematopoiesis, is highly www.selleckchem.com/products/U0126.html expressed in immature hematopoietic cells and its expression is down regulated upon differentiation. Moreover, enforced expres sion of normal and Inhibitors,Modulators,Libraries activated forms of MYB can sup press differentiation and maintain proliferation of hematopoietic cells. For these reasons, most work on MYB has focused on its role in normal and leukemic hematopoiesis. However, there is increasing evidence for a role of MYB in colonic epithelial cell differentiation and homeostasis, and nota bly, in colon cancer.

The Inhibitors,Modulators,Libraries pattern of MYB expression in normal colonic crypts suggests that, similarly to the hematopoietic system, expression is high in immature, rapidly proliferating cells, and decreases with differentia tion and maturation, whereas reduced MYB activity perturbs colonic epithelial proliferation, differentiation and viability. The involvement of MYB in epithelial tumors was first suggested by the amplification of MYB in certain colon carcinoma derived cell lines, and by its expression in a substantial proportion of tumors. Moreover MYB expression in colon tumors corre lates with poor clinical prognosis, and an important transcriptional regulatory region of MYB is frequently mutated in this disease. Furthermore, MYB is required for colon carcinoma cell proliferation, and is down regulated during differentiation of these cells while, conversely, ectopic MYB expression can suppress their differentiation.

By contrast, much less is known about the functions of MYB in mammary epithelial cells. Nevertheless, Inhibitors,Modulators,Libraries it has been shown that MYB is expressed at relatively high levels in estrogen receptor positive breast cancers and tumor cell lines. Moreover we, and others have previously shown that MYB is a direct target of estrogen Inhibitors,Modulators,Libraries ER signaling, and that MYB expression in breast cancer cells is regulated by transcriptional attenuation within its first intron. Importantly, we have also recently shown that MYB is required for the proliferation of ER positive, but not ER negative, breast cancer cell lines, identifying for the first time a functional role for MYB in breast cancer.

In addition, Fang et al reported a prolactin inducible association between MYB and Stat5a, and that a number of Stat5a responsive pro moters such as that of the CISH gene are further Inhibitors,Modulators,Libraries stimu lated by MYB. Their results suggested that MYB may act as a coactivator for Stat5a, and also supported a prolifera tive function for MYB in human breast cancer. To further understand selleckchem Imatinib Mesylate the function of MYB in breast cancer and in mammary epithelial cells gener ally, we have now investigated its role in the differentia tion of these cells.

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