Evidence map›Paper›PMID 28827783›Full record

ArticleScientific reports2017

Ccdc3: A New P63 Target Involved in Regulation Of Liver Lipid Metabolism.

Wenjuan Liao, Hongbing Liu, Yiwei Zhang, Ji Hoon Jung, Jiaxiang Chen, Xiaohua Su, Yeong C Kim, Elsa R Flores, San Ming Wang, Malwina Czarny-Ratajczak and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
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  13. Article
  14. CCDC3 Gene Regulates the Proliferation of Breast Cancer Cells.Bulletin of experimental biology and medicine · 2023
    Article
  15. Article
  16. The p53 Family: A Role in Lipid and Iron Metabolism.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. Control of metabolism by p53 - Cancer and beyond.Biochimica et biophysica acta. Reviews on cancer · 2018
    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

13 authors at 5 institutions in 3 countries.

Wenjuan LiaoDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Hongbing LiuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Yiwei ZhangDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Ji Hoon JungDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Jiaxiang ChenDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Xiaohua SuDepartment of Molecular Oncology, Cancer Biology and Evolution Program, H. Lee Moffitt Cancer Center, Tampa, Florida, USA.
Yeong C KimDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, 68198, NE, USA.ORCID 0000-0002-4526-067X
Elsa R FloresDepartment of Molecular Oncology, Cancer Biology and Evolution Program, H. Lee Moffitt Cancer Center, Tampa, Florida, USA.
San Ming WangDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, 68198, NE, USA.ORCID 0000-0002-2172-1320
Malwina Czarny-RatajczakDepartment of Medicine, Center for Aging, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Wen LiLaboratory of General Surgery, The First Affiliated Hospital, Sun Yatsen University, Guangzhou, Guangdong, 510080, P.R. China.
Shelya X ZengDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA. szeng@tulane.edu.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA. hlu2@tulane.edu.
Tulane University · USMoffitt Cancer Center · USSun Yat-sen University · CNUniversity of Macau · MOUniversity of Nebraska Medical Center · US

Funding

The role of the CMV-associated reactive oxygen species in age-relatedP20GM103629 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI JAZWINSKI, S MICHAL · 2012 to 2021
$22.4M
Identification of non-coding RNAs to therapeutically target undruggable pathways in metastatic lung adenocarcinoma and squamous cell carcinomaR35CA197452 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FLORES, ELSA R · 2016 to 2022
$6.4M
The Role of Ribosomal Proteins in the P53-MDM2 PathwayR01CA095441 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2002 to 2021
$5.1M
Role of the AMPK-MDMX-p53 pathway in cancerR01CA127724 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2007 to 2019
$3.0M
Digital Nanoplasmonic Quantification of Tumor-derived Extracellular Vesicles in Plasma MicrosamplesU01CA252965 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI HU, TONY Y., LU, HUA · 2020 to 2024
$3.0M
Dual Targeting of the p53 pathway for development of anti-cancer therapyR01CA172468 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2012 to 2016
$1.5M
Role of TFIIS.h in regulation of p53 responsive apoptosis and tumor suppressionR21CA201889 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2016 to 2017
$360k
Targeting GRP78 for p53 activation as anti-cancer therapyR21CA190775 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2015 to 2016
$360k
NCI NIH HHS R01 CA095441NCI NIH HHS R01 CA127724NCI NIH HHS R01 CA172468NCI NIH HHS R21 CA190775NCI NIH HHS R21 CA201889NCI NIH HHS R35 CA197452NCI NIH HHS U01 CA252965NIGMS NIH HHS P20 GM103629
6 · The paper itself

Abstract

TAp63, a member of the p53 family, has been shown to regulate energy metabolism. Here, we report coiled coil domain-containing 3 (CCDC3) as a new TAp63 target. TAp63, but not ΔNp63, p53 or p73, upregulates CCDC3 expression by directly binding to its enhancer region. The CCDC3 expression is markedly reduced in TAp63-null mouse embryonic fibroblasts and brown adipose tissues and by tumor necrosis factor alpha that reduces p63 transcriptional activity, but induced by metformin, an anti-diabetic drug that activates p63. Also, the expression of CCDC3 is positively correlated with TAp63 levels, but conversely with ΔNp63 levels, during adipocyte differentiation. Interestingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsaturated fatty acids, but decreases ceramide in the cells. CCDC3 alleviates glucose intolerance, insulin resistance and steatosis formation in transgenic CCDC3 mice on high-fat diet (HFD) by reducing the expression of hepatic PPARγ and its target gene CIDEA as well as other genes involved in de novo lipogenesis. Similar results are reproduced by hepatic expression of ectopic CCDC3 in mice on HFD. Altogether, these results demonstrate that CCDC3 modulates liver lipid metabolism by inhibiting liver de novo lipogenesis as a downstream player of the p63 network.

Indexed as

Gene Expression RegulationLipid MetabolismAdipocytesAnimalsCells, CulturedEnhancer Elements, GeneticFibroblastsLiverMiceMice, KnockoutPhosphoproteinsProtein BindingProteinsTrans-ActivatorsCCDC3 protein, mousePhosphoproteinsProteinsTrans-ActivatorsTrp63 protein, mouse

Identifiers

PMID28827783
PMCPMC5566403
OpenAlexW2625042870

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.