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Novel Lobophorins Inhibit Oral Cancer Cell Growth and Induce Atf4- and Chop-Dependent Cell Death in Murine Fibroblasts

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Date
2015-07-06
Author
Cruz, Patricia G.
Fribley, Andrew M.
Miller, Justin R.
Larsen, Martha J.
Schultz, Pamela J.
Jacob, Renju T.
Tamayo Castillo, Giselle
Kaufman, Randal J.
Sherman, David H.
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Abstract
As part of the International Cooperative Biodiversity Groups (ICBG) Program, we were interested in identifying biologically active unfolded protein response (UPR) inducing compounds from marine microorganisms isolated from Costa Rican biota. With this aim in mind we have now generated more than 33,000 unique prefractionated natural product extracts from marine and terrestrial organisms that have been submitted to the Center of Chemical Genomics (CCG) at the University of Michigan for high throughput screening (HTS). An effective complementary cell-based assay to identify novel modulators of UPR signaling was used for screening extracts. Active fractions were iteratively subjected to reverse-phase HPLC chromatographic analysis, and together with lobophorin A, B, E, and F (1–4), three new lobophorin congeners, designated as CR1 (5), CR2 (6), and CR3 (7) were isolated. Herein, we report that secondary assays revealed that the new lobophorins induced UPR-associated gene expression, inhibited oral squamous cell carcinoma cell growth, and led to UPR-dependent cell death in murine embryonic fibroblast (MEF) cells.
URI
http://hdl.handle.net/10669/76886
External link to the item
10.1021 / acsmedchemlett.5b00127
https://pubs.acs.org/doi/10.1021/acsmedchemlett.5b00127
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  • Repositorios universitarios

  • Repositorio del SIBDI-UCR
  • Biblioteca Digital del CIICLA
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  • Biblioteca Digital Carlos Melendez (CIHAC)
  • Repositorio de Fotografías
  • Colección de videos de UPA-VAS
  • Sitios recomendados

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  • Scientific Electronic Library Online (SciELO)
  • Directory of Open Access Journals (DOAJ)
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Repositorio Institucional de la Universidad de Costa Rica. Algunos derechos reservados. Este repositorio funciona con DSpace.
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