Evidence map›Paper›PMID 25057912›Full record

ArticlePloS one2014

Lactoferrin deficiency promotes colitis-associated colorectal dysplasia in mice.

Qiurong Ye, Ying Zheng, Songqing Fan, Zailong Qin, Nan Li, Anliu Tang, Feiyan Ai, Xuemei Zhang, Yanhui Bian, Wei Dang and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Deficiency of Lactoferrin aggravates lipopolysaccharide-induced acute inflammation via recruitment macrophage in mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
    Article
  4. Review
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  15. Article
  16. Mouse Models and Tools for theFrontiers in immunology · 2019
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

17 authors at 3 institutions in 1 country.

Qiurong YeHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Ying ZhengCenter for Medical Research, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Songqing FanDepartment of Pathology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zailong QinHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Nan LiDepartment of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Anliu TangDepartment of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Feiyan AiDepartment of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuemei ZhangDepartment of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yanhui BianHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Wei DangHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Jing HuangHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Ming ZhouHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Yanhong ZhouHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Wei XiongHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Qun YanDepartment of Laboratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jian MaHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Guiyuan LiHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonresolving inflammatory processes affect all stages of carcinogenesis. Lactoferrin, a member of the transferrin family, is involved in the innate immune response and anti-inflammatory, anti-microbial, and anti-tumor activities. We previously found that lactoferrin is significantly down-regulated in specimens of nasopharyngeal carcinoma (NPC) and negatively associated with tumor progression, metastasis, and prognosis of patients with NPC. Additionally, lactoferrin expression levels are decreased in colorectal cancer as compared with normal tissue. Lactoferrin levels are also increased in the various phases of inflammation and dysplasia in an azoxymethane-dextran sulfate sodium (AOM-DSS) model of colitis-associated colon cancer (CAC). We thus hypothesized that the anti-inflammatory function of lactoferrin may contribute to its anti-tumor activity. Here we generated a new Lactoferrin knockout mouse model in which the mice are fertile, develop normally, and display no gross morphological abnormalities. We then challenged these mice with chemically induced intestinal inflammation to investigate the role of lactoferrin in inflammation and cancer development. Lactoferrin knockout mice demonstrated a great susceptibility to inflammation-induced colorectal dysplasia, and this characteristic may be related to inhibition of NF-κB and AKT/mTOR signaling as well as regulation of cell apoptosis and proliferation. Our results suggest that the protective roles of lactoferrin in colorectal mucosal immunity and inflammation-related malignant transformation, along with a deficiency in certain components of the innate immune system, may lead to serious consequences under conditions of inflammatory insult.

Indexed as

AnimalsApoptosisAzoxymethaneCell ProliferationColitisColonic NeoplasmsDextran SulfateDisease Models, AnimalDown-RegulationGene Knockout TechniquesHumansInflammationLactoferrinMaleMiceNF-kappa BAzoxymethaneDextran SulfateLactoferrinLTF protein, humanLtf protein, mouseNF-kappa B

Identifiers

PMID25057912
PMCPMC4110006
OpenAlexW1977047382

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.