Evidence map›Paper›PMID 28455956›Full record

ArticleOncotarget2017

Targeting AXL overcomes resistance to docetaxel therapy in advanced prostate cancer.

Jian-Zhong Lin, Zeng-Jun Wang, Wei De, Ming Zheng, Wei-Zhang Xu, Hong-Fei Wu, Alex Armstrong, Jia-Geng Zhu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. Review
  5. Targeting AXL Inhibits the Growth and Metastasis of Prostate Cancer in Bone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  6. Review
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  15. Review
  16. Article
  17. AXL Inhibitors: Status of Clinical Development.Current oncology reports · 2023
    Review
  18. Article
  19. Article
  20. Review
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

8 authors at 3 institutions in 2 countries.

Jian-Zhong LinDepartment of Urology, BenQ Medical Center, Nanjing Medical University, Nanjing, China.
Zeng-Jun WangDepartment of Urology, The First Clinical College of Nanjing Medical University, Nanjing, China.
Wei DeDepartment of Biochemistry and Molecular biology, Nanjing Medical University, Nanjing, China.
Ming ZhengDepartment of Urology, The First Clinical College of Nanjing Medical University, Nanjing, China.
Wei-Zhang XuJiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, China.
Hong-Fei WuDepartment of Urology, BenQ Medical Center, Nanjing Medical University, Nanjing, China.
Alex ArmstrongDepartment of Pharmacology, University of Manchester, Manchester, England.
Jia-Geng ZhuDepartment of Urology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNJiangsu Cancer Hospital · CNUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to docetaxel is a major clinical problem in advanced prostate cancer. The overexpression of AXL receptor tyrosine kinase (AXL) has been correlated with chemotherapeutic drug resistance. However, the role of AXL expression in docetaxel resistance in prostate cancer is yet unclear. In this study, we demonstrate that AXL is overexpressed and activated independent of Gas6 in docetaxel-resistant prostate cancer cells (PC3-DR and DU145-DR). Moreover, we show that forced overexpression of AXL in PC3 and DU145 cells is sufficient to induce resistance to docetaxel in these cell lines. Notably, genetic or pharmacologic inhibition of AXL in the resistant models suppressed cell proliferation, migration, invasion, and tumor growth, and these effects were significantly augmented when AXL inhibition was combined with docetaxel treatment. Mechanistically, we found that AXL inhibition led to reversion of the epithelial-mesenchymal transition (EMT) phenotype and decreased the expression of ATP-binding cassette B1 (ABCB1). Overall, our results identify AXL as an important mediator of docetaxel resistance in prostate cancer. We propose that AXL-targeted therapy, in combination with docetaxel, has the potential to improve the response to docetaxel therapy and reduce resistance induced by prolonged docetaxel therapy in prostate cancer.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisAxl Receptor Tyrosine KinaseBenzocycloheptenesCell Line, TumorDocetaxelDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMice, NudePiperazinesProstatic NeoplasmsProtein Kinase InhibitorsamuvatinibAxl Receptor Tyrosine KinasebemcentinibBenzocycloheptenesDocetaxelPiperazinesProtein Kinase InhibitorsProto-Oncogene ProteinsPyrimidinesReceptor Protein-Tyrosine KinasesTaxoidsThioureaTriazolesATP-binding cassette B1 (ABCB1)AXLdocetaxel resistanceepithelial-mesenchymal transition (EMT)prostate cancer

Identifiers

PMID28455956
PMCPMC5522277
OpenAlexW2607286302

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.