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Mitochondrial Carrier Homolog 2 (MTCH2) Regulates the Differentiation of AML Cells By Controlling Pyruvate Entry into the Mitochondria, Nuclear Localization of Pyruvate Dehydrogenase Complex and H3 and H4 Histone Acetylation

2017· article· en· W2785287594 on OpenAlexaff
Dilshad H. Khan, Michael Mullokandov, Yan Wu, Marcela Gronda, Rose Hurren, Xiaoming Wang, Neil MacLean, Danny V. Jeyaraju, Guozhou Xu, Rob C. Laister, Zachary Blatman, Troy Ketela, Mark D. Minden, Atan Gross, Aaron D. Schimmer

Bibliographic record

VenueBlood · 2017
Typearticle
Languageen
FieldMedicine
TopicAcute Myeloid Leukemia Research
Canadian institutionsPrincess Margaret Cancer CentreUniversity Health Network
Fundersnot available
KeywordsBiologyHaematopoiesisCell biologyStem cellMitochondrionGene knockdownMolecular biologyCancer researchCell cultureGenetics

Abstract

fetched live from OpenAlex

Abstract Mitochondrial carrier homolog 2 (MTCH2) is a mitochondrial outer membrane protein that functions as a receptor for pro-apoptotic BID. MTCH2 also regulates metabolism through undefined mechanisms. We identified MTCH2 as essential for AML growth and viability in a CRISPR screen. OCI-AML2 leukemia cells overexpressing CAS9 were transduced with a library of 91,320 sgRNAs in barcoded lentiviral vectors. We focused on the gRNA that targeted the 1050 mitochondrial proteins and identified MTCH2 within the top 1% of hits. We validated this finding using two individual sgRNAs, where knockout of MTCH2 reduced the growth and viability of CAS9-OCI-AML2 cells by >75%. Additionally, knockdown of MTCH2 with shRNA reduced growth and viability of OCI-AML2 (>90%), TEX (>80%), U937 (>65%), and HL60 (>75%) leukemia cells. Knockdown of MTCH2 targeted the leukemia initiating cells as it abrogated engraftment of TEX cells into immune deficient mice. We also infected hematopoietic cells from wild type and MTCH2 flox/flox Vav1-cre mice with the MLL-AF9 oncogene. Knockout of MTCH2 decreased the leukemogenic potential of these cells and increased survival of the mice. In contrast, knockout of MTCH2 has more subtle effects on normal murine hematopoiesis. flox/flox Vav1-cre MTCH2 knockout mice had normal peripheral blood counts, but a ~15% reduction in the abundance of hematopoietic stem cells with a slight increase in the restricted progenitor populations (Maryanovich et al, Nat Comm 2015). Murine hematopoietic cells from MTCH2 -/- mice have increased mitochondrial mass and increased oxidative phosphorylation. Yet, no changes in basal oxygen consumption, mitochondrial ROS, or respiratory chain activity were seen in AML cells after MTCH2 knockdown. We examined changes in gene expression by RNA-sequencing in OCI-AML-2 cells after MTCH2 knockdown. MTCH2 knockdown increased expression of genes involved in cellular differentiation and decreased genes that maintain stemness. Therefore, we analyzed differentiation of AML cells after MTCH2 knockdown and demonstrated increased non-specific esterase staining and increased expression of CD cell surface markers associated with differentiation. In lung cancer mitochondrial stress induces the translocation of pyruvate dehydrogenase (PDH) from the mitochondria to the nucleus, where it increases conversion of pyruvate to Acetyl CoA which, in turn, acetylates histones. Therefore, we examined changes in PDH localization and histone acetylation after MTCH2 knockdown in OCI-AML-2 and TEX cells. MTCH2 knockdown decreased mitochondrial pyruvate, increased nuclear localization of pyruvate dehydrogenase complex (PDH) and increased acetylation of H3 and H4 histones. Over-expression of the PDH E2 subunit with a nuclear localizing signal mimicked MTCH2 knockdown and decreased cell growth, induced differentiation, and increased H3 and H4 histone acetylation in. Likewise, the acetyltransferase inhibitor, C646, abrogated the effects of MTCH2 knockdown on histone acetylation, growth and differentiation. We also demonstrated that knockdown of MTCH2 decreased levels of mitochondrial pyruvate in OCI-AML-2 cells. The entry of pyruvate into the mitochondria is regulated by the Mitochondrial Pyruvate Carrier (MPC). Therefore, we treated AML cells (OCI-AML2, TEX, HL60, and 8227) with the selective MPC inhibitor UK5099. UK5099 mimicked the effects of MTCH2 knockdown and decreased mitochondrial levels of pyruvate, reduced cell growth and viability, increased levels of acetylated histones, increased nuclear levels of PDH and promoted differentiation of AML cells. Treatment of mice with UK5099 (40mg/kg) decreased growth of OCI-AML2 xenografts. Finally, UK5099 induced cell death by Annexin V/PI staining in undifferentiated primary AML cells, but differentiated primary AML cells (by morphology and CD marker staining) and normal hematopoietic cells were more resistant. In summary, inhibiting entry of pyruvate into the mitochondria is a new mechanism to regulate differentiation of AML cells and stem cells by increasing PDH localization to the nucleus and histone acetylation. Thus, MTCH2 or MPC inhibitors may be novel therapeutics agents for AML. Disclosures Schimmer: Medivir: Research Funding; Takeda Pharmaceuticals: Research Funding; Novartis Pharmaceuticals: Honoraria.

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 machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation 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 score0.002
Threshold uncertainty score0.007

Distilled classifier scores by category (both heads)

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)0.0020.000

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 head0.010
GPT teacher head0.258
Teacher spread0.247 · 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 source (direct Gemma or distilled Codex), 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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Citations1
Published2017
Admission routes1
Has abstractyes

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