Evidence map›Paper›PMID 27034233›Full record

ArticleCancer immunology, immunotherapy : CII2016

Endostatin inhibits the growth and migration of 4T1 mouse breast cancer cells by skewing macrophage polarity toward the M1 phenotype.

Hua Guo, Yanan Liu, Junlian Gu, Yue Wang, Lianqin Liu, Ping Zhang, Yang Li

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. An obligatory anaerobicOncology letters · 2018
    Article
  11. Article
  12. Article
  13. 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

7 authors at 2 institutions in 1 country.

Hua GuoDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China.
Yanan LiuDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China.
Junlian GuDepartment of Pathology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, 250013, Shandong, People's Republic of China.
Yue WangDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China.
Lianqin LiuDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China.
Ping ZhangDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China.
Yang LiDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, School of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, People's Republic of China. lyang@jlu.edu.cn.
Jilin University · CNShandong Provincial QianFoShan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenotypic diversity of tumor-associated macrophages (TAMs) increases with tumor development. One of the hallmarks of malignancy is the polarization of TAMs from a pro-immune (M1) phenotype to an immunosuppressive (M2) phenotype. However, the molecular basis of this process is still unclear. Endostatin is a powerful inhibitor of angiogenesis capable of suppressing tumor growth and metastasis. Here, we demonstrate that endostatin induces RAW264.7 cell polarization toward the M1 phenotype in vitro. Endostatin has no effect on TAM numbers in vivo, but results in an increased proportion of F4/80(+)Nos2(+) cells and a decreased proportion of F4/80(+)CD206(+) cells. Overexpression of endostatin in RAW264.7 cells resulted in a decrease in the phosphorylation of STAT3, an increase in expression of vascular endothelial growth factor A and placental growth factor, and an increase in the phosphorylation of STAT1, IκBα and p65 proteins compared with controls. These results indicate that endostatin regulates macrophage polarization, promoting the M1 phenotype by targeting NF-κB and STAT signaling.

Indexed as

PhenotypeAnimalsAntineoplastic AgentsBiomarkersBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalEndostatinsFemaleGene ExpressionMacrophagesMiceTumor BurdenAntineoplastic AgentsBiomarkersEndostatins4T1EndostatinMacrophage polarizationTAM

Identifiers

PMID27034233
PMCPMC11028708
OpenAlexW2319851659

What OpenQuestion holds

Textmetadata
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.