Evidence map›Paper›PMID 24627480›Full record

ArticleThe Journal of biological chemistry2014

Blockade of Fas signaling in breast cancer cells suppresses tumor growth and metastasis via disruption of Fas signaling-initiated cancer-related inflammation.

Qiuyan Liu, Qinchun Tan, Yuanyuan Zheng, Kun Chen, Cheng Qian, Nan Li, Qingqing Wang, Xuetao Cao

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Apoptotic and Nonapoptotic Activities of Pterostilbene against Cancer.International journal of molecular sciences · 2018
    Review
  12. Interleukin-6Frontiers in immunology · 2017
    Article
  13. Inflammasomes in Inflammation-Induced Cancer.Frontiers in immunology · 2017
    Review
  14. Article
  15. Tagging staphylococcal enterotoxin B (SEB) with TGFaL3 for breast cancer therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
  17. Highlights on mechanisms of drugs targeting MDSCs: providing a novel perspective on cancer treatment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  18. The role of CD95 and CD95 ligand in cancer.Cell death and differentiation · 2015
    Review
  19. Article
  20. Microbiome, inflammation, and cancer.Cancer journal (Sudbury, Mass.)
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Qiuyan LiuNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China,. Electronic address: liuqy@immunol.org.
Qinchun TanInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China, and.
Yuanyuan ZhengNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Kun ChenInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China, and.
Cheng QianNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Nan LiNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China, and.
Xuetao CaoNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China,; Institute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China, and; National Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China. Electronic address: caoxt@immunol.org.
Second Military Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms for cancer-related inflammation remain to be fully elucidated. Non-apoptotic functions of Fas signaling have been proposed to play an important role in promoting tumor progression. It has yet to be determined if targeting Fas signaling can control tumor progression through suppression of cancer-related inflammation. In the current study we found that breast cancer cells with constitutive Fas expression were resistant to apoptosis induction by agonistic anti-Fas antibody (Jo2) ligation or Fas ligand cross-linking. Higher expression of Fas in human breast cancer tissue has been significantly correlated with poorer prognosis in breast cancer patients. To determine whether blockade of Fas signaling in breast cancer could suppress tumor progression, we prepared an orthotopic xenograft mouse model with mammary cancer cells 4T1 and found that blockade of Fas signaling in 4T1 cancer cells markedly reduced tumor growth, inhibited tumor metastasis in vivo, and prolonged survival of tumor-bearing mice. Mechanistically, blockade of Fas signaling in cancer cells significantly decreased systemic or local recruitment of myeloid derived suppressor cells (MDSCs) in vivo. Furthermore, blockade of Fas signaling markedly reduced IL-6, prostaglandin E2 production from breast cancer cells by impairing p-p38, and activity of the NFκB pathway. In addition, administration of a COX-2 inhibitor and anti-IL-6 antibody significantly reduced MDSC accumulation in vivo. Therefore, blockade of Fas signaling can suppress breast cancer progression by inhibiting proinflammatory cytokine production and MDSC accumulation, indicating that Fas signaling-initiated cancer-related inflammation in breast cancer cells may be a potential target for treatment of breast cancer.

Indexed as

AnimalsAntibodies, NeoplasmBreast NeoplasmsCell Line, TumorDinoprostonefas ReceptorFemaleHeterograftsHumansInflammationInterleukin-6Mammary Neoplasms, AnimalMiceMice, Inbred BALB CNeoplasm MetastasisNeoplasm ProteinsAntibodies, NeoplasmDinoprostoneFAS protein, humanFas protein, mousefas ReceptorIL6 protein, humanInterleukin-6Neoplasm ProteinsNF-kappa BBreast CancerFasIL-6InflammationMDSCPGE2ProstaglandinsTumor Metastases

Identifiers

PMID24627480
PMCPMC4036287
OpenAlexW2075885420

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.