Evidence map›Paper›PMID 32111229›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

FKBP9 promotes the malignant behavior of glioblastoma cells and confers resistance to endoplasmic reticulum stress inducers.

Huizhe Xu, Peng Liu, Yumei Yan, Kun Fang, Dapeng Liang, Xiukun Hou, Xiaohong Zhang, Songyan Wu, Jianmei Ma, Ruoyu Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. FKBP9 enhances IGF2BP1-mediated mJHEP reports : innovation in hepatology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cyclophilin A/CD147 Interaction: A Promising Target for Anticancer Therapy.International journal of molecular sciences · 2022
    Review
  18. Personalized 3-Gene Panel for Prostate Cancer Target Therapy.Current issues in molecular biology · 2022
    Article
  19. Article
  20. 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

13 authors at 5 institutions in 1 country.

Huizhe XuInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Peng LiuDepartment of General Surgery, Shenzhen University General Hospital, No. 1098, Xueyuan avenue, Shenzhen, 518055, China.
Yumei YanThe First Department of Ultrasound, The First Affiliated Hospital, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116021, Liaoning Province, China.
Kun FangInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Dapeng LiangInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Xiukun HouThe First Department of Ultrasound, The First Affiliated Hospital, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116021, Liaoning Province, China.
Xiaohong ZhangInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Songyan WuInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Jianmei MaDepartment of Anatomy, Dalian Medical University, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China.
Ruoyu WangDepartment of Oncology, Affiliated Zhongshan Hospital of Dalian University, No.6 Jiefang Street, Dalian, 116001, Liaoning Province, China. wangruoyu1963@163.com.
Tao LiDepartment of Neurosurgery, The First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, Liaoning Province, China. litaoxjtu@163.com.
Haozhe PiaoDepartment of Neurosurgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning Province, China. piaohaozhe@cancerhosp-ln-cmu.com.
Songshu MengInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, 9 Lvshun Road South, Dalian, 116044, Liaoning Province, China. ssmeng@dmu.edu.cn.
Dalian Medical University · CNAffiliated Zhongshan Hospital of Dalian University · CNFirst Affiliated Hospital of Dalian Medical University · CNLiaoning Cancer Hospital & Institute · CNShenzhen University · CN

Funding

Basic Scientific Research Projects of Institutions of Higher Learning of Liaoning Province LQ2017012National Natural Science Foundation of China 81572707National Natural Science Foundation of China 81772973Natural Science Foundation of Liaoning Province 20170540256
6 · The paper itself

Abstract

backgroundFK506-binding protein 9 (FKBP9) is amplified in high-grade gliomas (HGGs). However, the roles and mechanism(s) of FKBP9 in glioma are unknown.

methodsThe expression of FKBP9 in clinical glioma tissues was detected by immunohistochemistry (IHC). The correlation between FKBP9 expression levels and the clinical prognosis of glioma patients was examined by bioinformatic analysis. Glioblastoma (GBM) cell lines stably depleted of FKBP9 were established using lentiviruses expressing shRNAs against FKBP9. The effects of FKBP9 on GBM cells were determined by cell-based analyses, including anchorage-independent growth, spheroid formation, transwell invasion assay, confocal microscopy, immunoblot (IB) and coimmunoprecipitation assays. In vivo tumor growth was determined in both chick chorioallantoic membrane (CAM) and mouse xenograft models.

resultsHigh FKBP9 expression correlated with poor prognosis in glioma patients. Knockdown of FKBP9 markedly suppressed the malignant phenotype of GBM cells in vitro and inhibited tumor growth in vivo. Mechanistically, FKBP9 expression induced the activation of p38MAPK signaling via ASK1. Furthermore, ASK1-p38 signaling contributed to the FKBP9-mediated effects on GBM cell clonogenic growth. In addition, depletion of FKBP9 activated the IRE1α-XBP1 pathway, which played a role in the FKBP9-mediated oncogenic effects. Importantly, FKBP9 expression conferred GBM cell resistance to endoplasmic reticulum (ER) stress inducers that caused FKBP9 ubiquitination and degradation.

conclusionsOur findings suggest an oncogenic role for FKBP9 in GBM and reveal FKBP9 as a novel mediator in the IRE1α-XBP1 pathway.

Indexed as

Drug Resistance, NeoplasmAnimalsBrain NeoplasmsCell Line, TumorCell SurvivalChick EmbryoChorioallantoic MembraneEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticGlioblastomaHEK293 CellsHumansMiceNeoplasm TransplantationPrognosisProteolysisFKBP9 protein, humanTacrolimus Binding ProteinsEndoplasmic reticulum (ER) stressFK506-binding protein 9GliomaIRE1α-XBP1Unfolded protein response (UPR)

Identifiers

PMID32111229
PMCPMC7048151
OpenAlexW3010144706

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.