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Abstract IA27: Exploiting the inhibition of cullin-RING-ligases in DSB repair as a therapeutic strategy

2017· article· en· W2604615965 on OpenAlexaboutno aff
Meredith A. Morgan

Bibliographic record

VenueMolecular Cancer Research · 2017
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicUbiquitin and proteasome pathways
Canadian institutionsnot available
Fundersnot available
KeywordsCullinUbiquitinDNA repair protein XRCC4DNA repairUbiquitin ligaseKu70BiologyCell biologyKu80Non-homologous end joiningDNA damageCamptothecinCancer researchDNAGeneticsBiochemistryDNA-binding proteinDNA mismatch repairTranscription factor

Abstract

fetched live from OpenAlex

Abstract While single component E3 ubiquitin ligases have established roles in DNA double-strand break (DSB) repair, the function of multicomponent cullin-RING-ligases (CRL) in DSB repair is only beginning to emerge. FBXW7 is a substrate recognition component of Skp1-Cullin1-F-box E3 ubiquitin ligases previously known only to regulate the proteasomal degradation of substrates such as Cyclin E and MCL1. Given that FBXW7 loss promotes genomic instability, we hypothesized that FBXW7 may have a direct function in DSB repair. To establish the functions of FBXW7 in DSB repair, we first demonstrated the rapid localization of FBXW7 to DSB sites in an ATM-dependent manner. Subsequently, we found that FBXW7 depletion impaired nonhomologous end-joining (NHEJ), but not homologous recombination (HR) repair, resulting in persistent radiation-induced DSBs. Investigation of the molecular mechanisms of FBXW7 in NHEJ revealed that FBXW7 interacts with and promotes K63-linked ubiquitination of XRCC4. This ubiquitination of XRCC4 promotes interaction between the XRCC4/XLF/LIG4 and DNAPK/KU70/KU80 complexes to facilitate NHEJ. To begin to therapeutically leverage this mechanism, strategies to both pharmacologically inhibit FBXW7-CRLs and to exploit FBXW7 mutations occurring in human cancers are being developed. To address the former, pevonedistat (MLN4924), an agent which inhibits CRLs via inhibition of cullin-neddylation, inhibits FBXW7-mediated XRCC4 ubiquitination and NHEJ. This activity leads to increased sensitivity of tumor cells to chemotherapy and radiation and represents a strategy that may be particularly effective in cancers with other DSB repair defects. As another strategy to leverage the mechanisms of FBXW7 in NHEJ, loss-of-function mutations in the WD domain of FBXW7 which occur frequently in human cancers are being explored. These mutations render cells defective in NHEJ and more sensitive to DNA damage. Thus, we hypothesize that inhibition of other DSB repair pathways (e.g. alternative-end-joining) may be an effective therapeutic strategy for FBXW7 mutant cancers. These novel mechanisms of NHEJ regulation as well as their implications in the treatment of human cancers with an emphasis on pancreatic and colorectal cancers will be discussed. This work was supported by NIH grants R01CA163895, P50CA130810, R01CA118762, R01CA156744, and R01CA171277. Citation Format: Meredith Morgan. Exploiting the inhibition of cullin-RING-ligases in DSB repair as a therapeutic strategy [abstract]. In: Proceedings of the AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; 2016 Nov 2-5; Montreal, QC, Canada. Philadelphia (PA): AACR; Mol Cancer Res 2017;15(4_Suppl):Abstract nr IA27.

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)0.001
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 score0.012
Threshold uncertainty score0.468

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
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 head0.105
GPT teacher head0.406
Teacher spread0.301 · 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".

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Citations0
Published2017
Admission routes1
Has abstractyes

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