Reduction of LRH-1 diminishes tumor burden in murine models of CRC; however, it is not known whether LRH-1 is required for tumorigenesis, for proliferation, or for both.
In this work, we address this question through sh RNA-mediated silencing of LRH-1 in established CRC cell lines.
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Beyond sexual functions, androgens exert their action in skin physiology and pathophysiology.
Skin cells are able to synthesize most active androgens from gonadal or adrenal precursors and the enzymes involved in skin steroidogenesis are implicated both in normal or pathological processes.
Xiang Werdich, MD, Ph D completed a fellowship in Ophthalmic Pathology under the direction of Frederick A. Cogan Laboratory of Ophthalmic Pathology at the Massachusetts Eye and Ear Infirmary.
She is now doing an additional clinical fellowship at the Infirmary.
Recent evidence points to a central role for the nuclear receptor liver receptor homolog-1 (LRH-1) in intestinal tumorigenesis.
Interaction of LRH-1 with the Wnt/β-catenin pathway, highly active in a critical subpopulation of CRC cells, underscores the importance of elucidating LRH-1's role in this disease.
LRH-1 m RNA knockdown results in significantly impaired proliferation in a cell line highly expressing the receptor and more modest impairment in a cell line with moderate LRH-1 expression.