Evidence map›Paper›PMID 25956904›Full record

ArticleGenes & development2015

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

Ho-Chou Tu, Sarah Schwitalla, Zhirong Qian, Grace S LaPier, Alena Yermalovich, Yuan-Chieh Ku, Shann-Ching Chen, Srinivas R Viswanathan, Hao Zhu, Reiko Nishihara and 10 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

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  18. MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis.International journal of molecular sciences · 2021
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 7 institutions in 1 country.

Ho-Chou TuDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA;
Sarah SchwitallaDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA;
Zhirong QianDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Grace S LaPierDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA;
Alena YermalovichDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA;
Yuan-Chieh KuThermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA;
Shann-Ching ChenThermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA;
Srinivas R ViswanathanDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA;
Hao ZhuChildren's Medical Center Research Institute, University of Texas Southwestern, Dallas, Texas 75390, USA;
Reiko NishiharaDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Kentaro InamuraDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Sun A KimDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Teppei MorikawaDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Kosuke MimaDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Yasutaka SukawaDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Juhong YangDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Gavin MeredithThermo Fisher Scientific, Incorporated, South San Francisco, California 94080, USA;
Charles S FuchsDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA;
Shuji OginoDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA; Harvard Medical School, Boston, Massachusetts 02115, USA; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
George Q DaleyDivision of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA; Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA; Howard Hughes Medical Institute, Boston, Massachusetts 02138, USA george.daley@childrens.harvard.edu.
Dana-Farber Cancer Institute · USHarvard Stem Cell Institute · USHarvard University · USThermo Fisher Scientific (United States) · USBoston Children's Hospital · USBrigham and Women's Hospital · USChildren's Medical Center · US

Funding

Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
Physician Scientist Training in Cancer ResearchT32CA009172 · NCI · DANA-FARBER CANCER INSTITUTE · PI Jennifer R Brown, James A. DeCaprio · 1985 to 2026
$17.1M
Impact of Celecoxib and Inflammation on Survival in Stage III Colon CancerR01CA169141 · NCI · YALE UNIVERSITY · PI FUCHS, CHARLES S · 2013 to 2018
$3.9M
Epigenetic Events and Colorectal Cancer EpidemiologyR01CA151993 · NCI · DANA-FARBER CANCER INST · PI OGINO, SHUJI · 2010 to 2014
$2.6M
Understanding the role of the lin28 paralogs and branching morphogenesisR01GM107536 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI DALEY, GEORGE Q · 2014 to 2017
$1.9M
Lifestyle, genetics and colonoscopy for colorectal cancer preventionK07CA190673 · NCI · DANA-FARBER CANCER INST · PI NISHIHARA, REIKO · 2014 to 2018
$609k
THE ROLE OF LIN28B IN WILMS TUMORF31CA186444 · NCI · BOSTON CHILDREN'S HOSPITAL · PI YERMALOVICH, ALENA · 2014 to 2015
$70k
Howard Hughes Medical InstituteNCI NIH HHS F31 CA186444NCI NIH HHS K07 CA190673NCI NIH HHS NIH F31 CA186444-01NCI NIH HHS NIH K07 CA190673NCI NIH HHS NIH P01CA127003NCI NIH HHS NIH RO1CA151993NCI NIH HHS P50 CA127003NCI NIH HHS R01 CA151993NCI NIH HHS R01 CA169141NCI NIH HHS T32 CA009172NIGMS NIH HHS NIH; R01GM107536NIGMS NIH HHS R01 GM107536
6 · The paper itself

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 (β-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.

Indexed as

Signal TransductionAdenocarcinomaAnimalsColorectal NeoplasmsGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessRNA-Binding ProteinsWnt ProteinsLin28A protein, humanLin-28 protein, mouseRNA-Binding ProteinsWnt Proteinscolorectal cancerinvasive adenocarcinomalet-7 miRNALIN28oncogene cooperationWNT

Identifiers

PMID25956904
PMCPMC4441054
OpenAlexW1853854707

What OpenQuestion holds

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LicenceCC BY-NC
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.