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Record W4362596380 · doi:10.1158/1538-7445.am2023-446

Abstract 446: LONP1 inhibition induces mitochondrial proteotoxic stress and is cytotoxic to acute myeloid leukemia cells

2023· article· en· W4362596380 on OpenAlexaff
Matthew Tcheng

Bibliographic record

VenueCancer Research · 2023
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicATP Synthase and ATPases Research
Canadian institutionsPrincess Margaret Cancer Centre
Fundersnot available
KeywordsBiologyMyeloid leukemiaCell biologyMitochondrionMyeloidGene knockdownHaematopoiesisStem cellCancer researchApoptosisGenetics

Abstract

fetched live from OpenAlex

Abstract Acute myeloid leukemia (AML) is a hematological malignancy characterized by the uncontrolled proliferation of abnormal myeloid precursors that fail to fully differentiate, resulting in the accumulation of malignant leukemic cells. High rates of nuclear-encoded protein synthesis, supporting increased proliferation rates, render leukemic cells reliant on increased proteolytic systems to clear misfolded proteins. Compared to non-transformed blood cells, AML cells and stem cells exhibit a unique metabolic phenotype characterized by increased mitochondrial mass and greater reliance on oxidative metabolism for survival and proliferation. To identify novel biological vulnerabilities in the mitochondrial proteome, we analyzed the DepMap (depmap.org) for essential mitochondrial genes in AML. Through this analysis, we identified the mitochondrial protease LONP1 as essential for a subset of AML and in the top 10% of essential genes for this disease. LONP1 is a nuclear-encoded AAA+ serine protease that resides in the mitochondrial matrix and maintains the mitochondrial proteome, mainly via the clearance of misfolded, unassembled or oxidatively-damaged proteins. However, its importance and function in AML has not been previously reported. Compared to normal hematopoietic cells, LONP1 mRNA was overexpressed in AML across three publicly available datasets while LONP1 protein was increased >2 fold in tested AML primary samples (N=16). Using shRNA and CRISPR gRNA, LONP1 knockdown and knockout reduced the growth and viability of OCI-AML2, OCI-M2, and NB4 cells. Mechanistically, genetic knockdown or knockout of LONP1 increased levels of insoluble, aggregated mitochondrial proteins including ClpP, TUFM, and NDUFA9 as measured by immunoblotting of soluble and insoluble protein fractions as well as by the fluorescence of the protein aggregation dye PROTEOSTAT by confocal microscopy. The accumulation of insoluble mitochondrial protein aggregates through LONP1 inhibition exploits an increased reliance on chaperone and protease systems due to abnormally high protein synthesis. This novel therapeutic avenue targets a unique metabolic vulnerability to eliminate AML cells. Citation Format: Matthew Tcheng. LONP1 inhibition induces mitochondrial proteotoxic stress and is cytotoxic to acute myeloid leukemia cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 446.

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 score0.017
Threshold uncertainty score0.736

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.001
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 head0.046
GPT teacher head0.381
Teacher spread0.335 · 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

Citations0
Published2023
Admission routes1
Has abstractyes

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