Evidence map›Paper›PMID 26122663›Full record

ArticleThe Journal of experimental medicine2015

Targeting phospholipase D1 attenuates intestinal tumorigenesis by controlling β-catenin signaling in cancer-initiating cells.

Dong Woo Kang, Chi Yeol Choi, Yong-Hee Cho, Huasong Tian, Gilbert Di Paolo, Kang-Yell Choi, Do Sik Min

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
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

31 citing papers in PubMed, 52 citations in OpenAlex.

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  13. Phospholipase Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021
    Review
  14. Article
  15. Article
  16. Phospholipase D1 and D2 Synergistically Regulate Thrombus Formation.International journal of molecular sciences · 2020
    Article
  17. Article
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  20. Review
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

7 authors at 4 institutions in 2 countries.

Dong Woo KangDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan 609-735, Republic of Korea Institute for Innovative Cancer Research, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
Chi Yeol ChoiDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan 609-735, Republic of Korea.
Yong-Hee ChoDepartment of Biotechnology, College of Life Science and Biotechnology, and Translational Research Center for Protein Function Control, Yonsei University, Seoul 120-749, Republic of Korea.
Huasong TianDivision of Solid Tumor Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065.
Gilbert Di PaoloDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032.
Kang-Yell ChoiDepartment of Biotechnology, College of Life Science and Biotechnology, and Translational Research Center for Protein Function Control, Yonsei University, Seoul 120-749, Republic of Korea Department of Biotechnology, College of Life Science and Biotechnology, and Translational Research Center for Protein Function Control, Yonsei University, Seoul 120-749, Republic of Korea.
Do Sik MinDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan 609-735, Republic of Korea Department of Biotechnology, College of Life Science and Biotechnology, and Translational Research Center for Protein Function Control, Yonsei University, Seoul 120-749, Republic of Korea minds@pusan.ac.kr.
Yonsei University · KRPusan National University · KRColumbia University Irving Medical Center · USMemorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of the Wnt target gene phospholipase D1 (PLD1) is up-regulated in various carcinomas, including colorectal cancer (CRC). However, the mechanistic significance of its elevated expression in intestinal tumorigenesis remains unknown. In this study, we show that genetic and pharmacological targeting of PLD1 disrupts spontaneous and colitis-associated intestinal tumorigenesis in Apc(Min/+) and azoxymethane/dextran sodium sulfate mice models. Intestinal epithelial cell-specific PLD1 overexpression in Apc(Min/+) mice accelerated tumorigenesis with increased proliferation and nuclear β-catenin levels compared with Apc(Min/+) mice. Moreover, PLD1 inactivation suppressed the self-renewal capacity of colon cancer-initiating cells (CC-ICs) by decreasing expression of β-catenin via E2F1-induced microRNA (miR)-4496 up-regulation. Ultimately, low expression of PLD1 coupled with a low level of CC-IC markers was predictive of a good prognosis in CRC patients, suggesting in vivo relevance. Collectively, our data reveal that PLD1 has a crucial role in intestinal tumorigenesis via its modulation of the E2F1-miR-4496-β-catenin signaling pathway. Modulation of PLD1 expression and activity represents a promising therapeutic strategy for the treatment of intestinal tumorigenesis.

Indexed as

AnimalsApoptosisAzoxymethanebeta CateninBlotting, WesternCarcinogenesisDextran SulfateDNA PrimersFlow CytometryHEK293 CellsHumansImmunohistochemistryImmunoprecipitationIn Situ Nick-End LabelingIntestinal NeoplasmsMiceAzoxymethanebeta CateninDextran SulfateDNA PrimersMicroRNAsMIRN4496 microRNA, humanPhospholipase Dphospholipase D1

Identifiers

PMID26122663
PMCPMC4516794
OpenAlexW2129303232

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.