Evidence map›Paper›PMID 27991933›Full record

ArticleOncogene2017

Cancer-FOXP3 directly activated CCL5 to recruit FOXP3

X Wang, M Lang, T Zhao, X Feng, C Zheng, C Huang, J Hao, J Dong, L Luo, X Li and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

139 citing papers in PubMed, 2 syntheses or guidelines pooled it, 232 citations in OpenAlex.

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79 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

15 authors at 5 institutions in 2 countries.

X WangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
M LangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
T ZhaoTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
X FengThe State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
C ZhengTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
C HuangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
J HaoTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
J DongDepartment of Nutrition and Food Hygiene, School of Public Health, Tianjin Medical University, Tianjin, China.
L LuoDepartment of Gynaecology, Hepingqu Gynaecology and Obsterics Hospital, Tianjin, China.
X LiTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
C LanTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
W YuTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
M YuDepartment of Nutrition and Food Hygiene, School of Public Health, Tianjin Medical University, Tianjin, China.
S YangPenn State College of Medicine, Hershey, PA, USA.
H RenTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China.
National Clinical Research · USTianjin Medical University Cancer Institute and Hospital · CNTianjin Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPenn State Milton S. Hershey Medical Center · US

Funding

Store-Operated Calcium Entry in Tumor Invasion and MetastasisR01CA175741 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI YANG, SHENGYU · 2014 to 2018
$1.7M
NCI NIH HHS R01 CA175741
6 · The paper itself

Abstract

Forkheadbox protein 3 (FOXP3), initially identified as a key transcription factor for regulatory T cells (Treg cells), was also expressed in many tumors including pancreatic ductal adenocarcinoma (PDAC). However, its role in PDAC progression remains elusive. In this study, we utilized 120 PDAC tissues after radical resection to detect cancer-FOXP3 and Treg cells by immunohistochemistry and evaluated clinical and pathological features of these patients. Cancer-FOXP3 was positively correlated with Treg cells accumulation in tumor tissues derived from PDAC patients. In addition, high cancer-FOXP3 expression was associated with increased tumor volumes and poor prognosis in PDAC especially combined with high levels of Treg cells. Overexpression of cancer-FOXP3 promoted the tumor growth in immunocompetent syngeneic mice but not in immunocompromised or Treg cell-depleted mice. Furthermore, CCL5 was directly trans-activated by cancer-FOXP3 and promoted the recruitment of Treg cells from peripheral blood to the tumor site in vitro and in vivo. This finding has been further reinforced by the evidence that Treg cells recruitment by cancer-FOXP3 was impaired by neutralization of CCL5, thereby inhibiting the growth of PDAC. In conclusion, cancer-FOXP3 serves as a prognostic biomarker and a crucial determinant of immunosuppressive microenvironment via recruiting Treg cells by directly trans-activating CCL5. Therefore, cancer-FOXP3 could be used to select patients with better response to CCL5/CCR5 blockade immunotherapy.

Indexed as

AdultAgedAnimalsCarcinoma, Pancreatic DuctalCells, CulturedChemokine CCL5Chemotaxis, LeukocyteFemaleForkhead Transcription FactorsHumansLymphocyte ActivationMaleMiceMice, Inbred C57BLMice, NudeMice, SCIDChemokine CCL5Forkhead Transcription FactorsFOXP3 protein, human

Identifiers

PMID27991933
PMCPMC5454319
OpenAlexW2565788901

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.