Evidence map›Paper›PMID 36397015›Full record

ArticleBMC cancer2022

CX3CL1 promotes cell sensitivity to ferroptosis and is associated with the tumor microenvironment in clear cell renal cell carcinoma.

Qiming Gong, Zhiting Guo, Wenjuan Sun, Xiuri Du, Yan Jiang, Fahui Liu

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Effects of DNA, RNA, and Protein Methylation on the Regulation of Ferroptosis.International journal of biological sciences · 2023
    Review
  16. Article
  17. 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

6 authors at 4 institutions in 3 countries.

Qiming Gong *Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No.18 Zhongshan Road, Baise, 533000, Guangxi, China.
Zhiting Guo *College of Biological Science and Engineering, Fuzhou University, Fuzhou, 350108, China.
Wenjuan SunDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, 61469, South Korea.
Xiuri DuDepartment of Rheumatology, Affiliated Hospital of Youjiang Medical University for Nationalities, No.18 Zhongshan Road, Baise, 533000, Guangxi, China.
Yan Jiang *Science Laboratory, Youjiang Medical University for Nationalities, No.98 Chengxiang Road, Baise, 533000, Guangxi, China. jiangyan9hr@yeah.net.
Fahui Liu *Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, 40530, Gothenburg, Sweden. liufahui005@163.com.
Affiliated Hospital of Youjiang Medical University for Nationalities · CNChonnam National University · KRFuzhou University · CNUniversity of Gothenburg · SE

Funding

Natural Science Foundation of Guangxi Province 2020JJB140078
6 · The paper itself

Abstract

backgroundAn increasing number of studies have demonstrated that CX3CL1 is involved in the development of tumors and may thus be considered a new potential therapeutic target for them. However, the function of CX3CL1 in clear cell renal cell carcinoma (ccRCC) remains poorly defined.

methodsThe pan-cancer expression pattern and prognostic value of CX3CL1 were evaluated in this study. Moreover, the relationship of CX3CL1 expression with the tumor microenvironment, especially the tumor immune microenvironment, was analyzed. Our analyses employed public repository data. Additionally, we generated stable CX3CL1-overexpressing 786-O cells to determine the role of CX3CL1 in vitro via cell viability and transwell assays. A xenograft tumor model was used to determine the role of CX3CL1 in vivo. The association between CX3CL1 and ferroptosis sensitivity of tumor cells was assessed using Ferrostatin-1.

resultsOur findings indicated the involvement of CX3CL1 in the occurrence and development of ccRCC by acting as a tumor suppressor. We also found that ccRCC patients with high CX3CL1 expression showed better clinical outcomes than those with low CX3CL1 expression. The findings of our epigenetic study suggested that the expression of CX3CL1 in ccRCC is correlated with its DNA methylation level. Furthermore, the CX3CL1 expression level was closely related to the infiltration level of CD8

conclusionsThis study revealed the role of CX3CL1 as a tumor suppressor in ccRCC. Our findings indicated that CX3CL1 plays a crucial role in regulating the ccRCC TME and is a potential predictor of immunotherapy outcomes in ccRCC. We also found that CX3CL1 can promote ferroptosis sensitivity in ccRCC cells.

Indexed as

Carcinoma, Renal CellFerroptosisKidney NeoplasmsCD8-Positive T-LymphocytesCell Line, TumorChemokine CX3CL1HumansTumor MicroenvironmentChemokine CX3CL1CX3CL1 protein, humanClear cell renal cell carcinomaCX3CL1FerroptosisImmunotherapyTumor microenvironment

Identifiers

PMID36397015
PMCPMC9670481
OpenAlexW4309467527

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.