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Record W2536913008 · doi:10.18632/oncotarget.12838

The intrinsically kinase-inactive EPHB6 receptor predisposes cancer cells to DR5-induced apoptosis by promoting mitochondrial fragmentation

2016· article· en· W2536913008 on OpenAlexafffundabout
Amr M. El Zawily, Behzad M. Toosi, Tanya Freywald, Vijaya Indukuri, Franco J. Vizeacoumar, Scot C. Leary, Andrew Freywald

Bibliographic record

VenueOncotarget · 2016
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCell death mechanisms and regulation
Canadian institutionsSaskatchewan Cancer AgencyUniversity of SaskatchewanRoyal University Hospital
FundersCanadian Institutes of Health ResearchCure Brain Cancer FoundationSaskatchewan Health Research Foundation
KeywordsCancer researchReceptor tyrosine kinaseMAPK/ERK pathwayKinaseCancer cellApoptosisBiologySignal transductionCancerCell biologyGenetics

Abstract

fetched live from OpenAlex

// Amr M. El Zawily 1, 2 , Behzad M. Toosi 1 , Tanya Freywald 3 , Vijaya V. Indukuri 4 , Franco J. Vizeacoumar 1, 3 , Scot C. Leary 4 , Andrew Freywald 1 1 Department of Pathology and Laboratory Medicine, College of Medicine, University of Saskatchewan, Royal University Hospital, Saskatoon, SK, S7N 0W8, Canada 2 Faculty of Science, Damanhour University, Damanhour, 22516, Egypt 3 Cancer Research, Saskatchewan Cancer Agency, Saskatoon, SK, S7N 5E5, Canada 4 Department of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada Correspondence to: Andrew Freywald, email: andrew.freywald@usask.ca Scot C. Leary, email: scot.leary@usask.ca Keywords: EPHB6, DRP1, mitochondrial dynamics, cancer, DR5 Received: August 19, 2016     Accepted: October 12, 2016     Published: October 24, 2016 ABSTRACT Death Receptor 5 (DR5) is a promising target for cancer therapy due to its ability to selectively induce apoptosis in cancer cells. However, the therapeutic usefulness of DR5 agonists is currently limited by the frequent resistance of malignant tumours to its activation. The identification of molecular mechanisms that determine outcomes of DR5 action is therefore crucial for improving the efficiency of DR5-activating reagents in cancer treatment. Here, we provide evidence that an intrinsically kinase-inactive member of the Eph group of receptor tyrosine kinases, EPHB6, induces marked fragmentation of the mitochondrial network in breast cancer cells of triple-negative origin, lacking expression of the estrogen, progesterone and HER2 receptors. Remarkably, this response renders cancer cells more susceptible to DR5-mediated apoptosis. EPHB6 action in mitochondrial fragmentation proved to depend on its ability to activate the ERK-DRP1 pathway, which increases the frequency of organelle fission. Moreover, DRP1 activity is also essential to the EPHB6-mediated pro-apoptotic response that we observe in the context of DR5 activation. These findings provide the first description of a member of the receptor tyrosine kinase family capable of producing a pro-apoptotic effect through the activation of ERK-DRP1 signaling and subsequent mitochondrial fragmentation. Our observations are of potential practical importance, as they imply that DR5-activating therapeutic approaches should be applied in a more personalized manner to primarily treat EPHB6-expressing tumours. Finally, our findings also suggest that the EPHB6 receptor itself may represent a promising target for cancer therapy, since EPHB6 and DR5 co-activation should support more efficient elimination of cancer cells.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.072
Threshold uncertainty score0.389

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.005
GPT teacher head0.245
Teacher spread0.240 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations14
Published2016
Admission routes3
Has abstractyes

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