Evidence map›Paper›PMID 31160603›Full record

ArticleExperimental & molecular medicine2019

EPHB6 mutation induces cell adhesion-mediated paclitaxel resistance via EPHA2 and CDH11 expression.

Sarah Yoon, Ji-Hye Choi, Sung Joo Kim, Eun-Ju Lee, Masaud Shah, Sangdun Choi, Hyun Goo Woo

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. May EPH/Ephrin Targeting Revolutionize Lung Cancer Treatment?International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. The EphB6 Receptor: Kinase-Dead but Very Much Alive.International journal of molecular sciences · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Observational
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

7 authors at 1 institution in 1 country.

Sarah YoonDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Ji-Hye ChoiDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Sung Joo KimDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Eun-Ju LeeDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Masaud ShahDepartment of Molecular Science and Technology, Ajou University, Suwon, Republic of Korea.
Sangdun ChoiDepartment of Molecular Science and Technology, Ajou University, Suwon, Republic of Korea.
Hyun Goo WooDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea. hg@ajou.ac.kr.
Ajou University · KR

Funding

Korea Health Industry Development Institute (KHIDI) H15C1551National Research Foundation of Korea (NRF) NRF-2015R1D1A4A01020022National Research Foundation of Korea (NRF) NRF-2017M3A9B6061509National Research Foundation of Korea (NRF) NRF-2017M3C9A6047620National Research Foundation of Korea (NRF) NRF-2017R1E1A1A01074733
6 · The paper itself

Abstract

Mutations affect gene functions related to cancer behavior, including cell growth, metastasis, and drug responses. Genome-wide profiling of cancer mutations and drug responses has identified actionable targets that can be utilized for the management of cancer patients. Here, the recapitulation of pharmacogenomic data revealed that the mutation of EPHB6 is associated with paclitaxel resistance in cancer cells. Experimental data confirmed that the EPHB6 mutation induces paclitaxel resistance in various cancer types, including lung, skin, and liver cancers. EPHB6 mutation-induced paclitaxel resistance was mediated by an interaction with EPHA2, which promotes c-Jun N-terminal kinase (JNK)-mediated cadherin 11 (CDH11) expression. We demonstrated that EPHB6-mutated cells acquire cell adhesion-mediated drug resistance (CAM-DR) in association with CDH11 expression and RhoA/focal adhesion kinase (FAK) activation. Targeted inhibition of EPHA2 or CDH11 reversed the acquired paclitaxel resistance, suggesting its potential clinical utility. The present results suggest that the EPHB6 mutation and its downstream EPHA2/JNK/CDH11/RhoA/FAK signaling axis are novel diagnostic and therapeutic targets for overcoming paclitaxel resistance in cancer patients.

Indexed as

Antineoplastic Agents, PhytogenicCadherinsCell Line, TumorDrug Resistance, NeoplasmEphrin-A2Gene Expression Regulation, NeoplasticHumansNeoplasmsPaclitaxelReceptor, EphA2Receptors, Eph FamilyAntineoplastic Agents, PhytogenicCadherinsEPHA2 protein, humanEPHB6 protein, humanEphrin-A2osteoblast cadherinPaclitaxelReceptor, EphA2Receptors, Eph Family

Identifiers

PMID31160603
PMCPMC6547695
OpenAlexW2947631923

What OpenQuestion holds

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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.