Evidence map›Paper›PMID 24362529›Full record

ArticleOncogene2015

Interleukin-17 produced by tumor microenvironment promotes self-renewal of CD133+ cancer stem-like cells in ovarian cancer.

T Xiang, H Long, L He, X Han, K Lin, Z Liang, W Zhuo, R Xie, B Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
4.5field-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

115 citing papers in PubMed, 195 citations in OpenAlex.

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  17. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
    Article
  18. Review
  19. Review
  20. Article

55 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

9 authors at 3 institutions in 1 country.

T XiangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
H LongInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
L HeInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
X HanInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
K LinInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Z LiangDepartment of Obstetrics and Gynecology, Southwest Hospital, Third Military Medical University, Chongqing, China.
W ZhuoInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
R Xie1] Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China [2] Department of Obstetrics and Gynecology, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
B Zhu1] Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China [2] Biomedical Analysis Center, Third Military Medical University, Chongqing, China.
Army Medical University · CNXinqiao Hospital · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory cytokines, components of cancer stem cells (CSCs) niche, could affect the characteristics of CSCs such as self-renewal and metastasis. Interleukin-17 (IL-17) is a new pro-inflammatory cytokine mainly produced by T-helper (Th17) cells and macrophages. The effects of IL-17 on the characteristics of CSCs remain to be explored. Here we first demonstrated a role of IL-17 in promoting the self-renewal of ovarian CD133(+) cancer stem-like cells (CSLCs). We detected IL-17-producing cells (CD4(+) cells and CD68(+) macrophages) in the niche of CD133(+)CSLCs. Meanwhile, there was IL-17 receptor expression on CD133(+)CSLCs derived from A2780 cell line and primary ovarian cancer tissues. By recombinant human IL-17 stimulation and IL-17 transfection, the growth and sphere formation capacities of ovarian CD133(+)CSLCs were significantly enhanced in a dose-dependent manner. Moreover, ovarian CD133(+)CSLCs transfected with IL-17 showed greater tumorigenesis capacity in nude mice. These data suggest that IL-17 promoted the self-renewal of ovarian CD133(+)CSLCs. Further investigation through gene profiling revealed that the stimulation function of IL-17 on self-renewal of ovarian CD133(+)CSLCs might be mediated by the nuclear factor (NF)-κB and p38 mitogen-activated protein kinases (MAPK) signaling pathway. NF-κB and p38 MAPK were activated by IL-17. More importantly, IL-17-promoted self-renewal was inhibited by specific inhibitors of NF-κB and p38 MAPK. Taken together, our data indicate that IL-17 contributed to ovarian cancer malignancy through promoting the self-renewal of CD133(+)CSLCs and that IL-17 and its signaling pathway might serve as therapeutic targets for the treatment of ovarian cancer.

Indexed as

AC133 AntigenAnimalsAntigens, CDCell Line, TumorFemaleGene Expression ProfilingGlycoproteinsHeterograftsHumansInterleukin-17MiceMice, NudeMice, SCIDNeoplastic Stem CellsOvarian NeoplasmsPeptidesAC133 AntigenAntigens, CDGlycoproteinsInterleukin-17PeptidesPROM1 protein, humanProm1 protein, mouse

Identifiers

PMID24362529
OpenAlexW1991345800

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.