Abstract
Correction: PERK Regulates the Proliferation and Development of Insulin-Secreting Beta-Cell Tumors in the Endocrine Pancreas of Mice
Highlights
In the small number of large encapsulated insulinomas that developed in Perk-deficient mice, we found a dramatic reduction in tumor vascularity compared to similar sized insulinomas in wild-type mice
We conclude that PERK has two roles in the development of beta-cell insulinomas, first to support rapid cell proliferation during the initial transition to islet hyperplasia and later to promote angiogenesis during the progression to late-stage encapsulated tumors
Tumor growth is dependent upon high rates of protein synthesis, and previous studies had shown that control of protein synthesis mediated by phosphorylation of the translation initiation factor eIF2a is important for tumor progression [1,2,3,4]
Summary
Tumor growth is dependent upon high rates of protein synthesis, and previous studies had shown that control of protein synthesis mediated by phosphorylation of the translation initiation factor eIF2a is important for tumor progression [1,2,3,4]. Previous studies have shown that tumors that lack PERK-mediated signaling tend to be smaller and this was found to be correlated with smaller hypoxic microenvironments [5,6,7]. The resultant tumors were found to be smaller and less vascular compared to control implants that were wild type for Perk [6,7] In these studies, the dramatic reduction in growth of the Perk-deficient tumors was attributed to increased rates of apoptotic cell death and impaired angiogenesis but, inexplicably, tumor cell proliferation rates were not examined [6,7]. In this report we examine the role of PERK in regulating proliferation and angiogenesis of transformed beta-cells in the development of insulinomas
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