NDLI: LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans.

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LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tu, Ho-Chou Schwitalla, Sarah Qian, Zhirong LaPier, Grace S. Yermalovich, Alena Ku, Yuan-Chieh Chen, Shann-Ching Viswanathan, Srinivas R. Zhu, Hao Nishihara, Reiko Inamura, Kentaro Kim, Sun A. Morikawa, Teppei Mima, Kosuke Sukawa, Yasutaka Yang, Juhong Meredith, Gavin Fuchs, Charles S. Ogino, Shuji Daley, George Q.
Description	Author Affiliation: Tu HC ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA); Schwitalla S ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA); Qian Z ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); LaPier GS ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA); Yermalovich A ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA); Ku YC ( Thermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA); Chen SC ( Thermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA); Viswanathan SR ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA); Zhu H ( Children's Medical Center Research Institute, University of Texas Southwestern, Dallas, Texas 75390, USA); Nishihara R ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Inamura K ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Kim SA ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Morikawa T ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Mima K ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Sukawa Y ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Yang J ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Meredith G ( Thermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA); Fuchs CS ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Ogino S ( Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA); Daley GQ ( Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA)
Abstract	Colorectal cancer (CRC) remains a major contributor to cancer-related mortality. LIN28A and LIN28B are highly related RNA-binding protein paralogs that regulate biogenesis of let-7 microRNAs and influence development, metabolism, tissue regeneration, and oncogenesis. Here we demonstrate that overexpression of either LIN28 paralog cooperates with the Wnt pathway to promote invasive intestinal adenocarcinoma in murine models. When LIN28 alone is induced genetically, half of the resulting tumors harbor Ctnnb1 (ß-catenin) mutation. When overexpressed in Apc(Min/+) mice, LIN28 accelerates tumor formation and enhances proliferation and invasiveness. In conditional genetic models, enforced expression of a LIN28-resistant form of the let-7 microRNA reduces LIN28-induced tumor burden, while silencing of LIN28 expression reduces tumor volume and increases tumor differentiation, indicating that LIN28 contributes to tumor maintenance. We detected aberrant expression of LIN28A and/or LIN28B in 38% of a large series of human CRC samples (n = 595), where LIN28 expression levels were associated with invasive tumor growth. Our late-stage CRC murine models and analysis of primary human tumors demonstrate prominent roles for both LIN28 paralogs in promoting CRC growth and progression and implicate the LIN28/let-7 pathway as a therapeutic target.
File Format	HTM / HTML
ISSN	08909369
e-ISSN	15495477
DOI	10.1101/gad.256693.114
Journal	Genes & Development
Issue Number	10
Volume Number	29
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2015-05-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Molecular Discipline Biology__semicolon__developmental Discipline Biology__semicolon__genetics__semicolon__cell Discipline Biology Adenocarcinoma Physiopathology Colorectal Neoplasms Rna-binding Proteins Metabolism Signal Transduction Wnt Proteins Animals Gene Expression Regulation, Neoplastic Mice Neoplasm Invasiveness Genetics Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Genetics Developmental Biology

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