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Record W3107924164

DNA Demethylase transforms normal cells into highly invasive and metastatic cancer cells: Identification and characterization of novel metastatic cancer targets, therapeutic intervention for these targets, and signaling pathways leading to DNA demethylation

2008· article· en· W3107924164 on OpenAlexaffabout
Stephen D. Andrews, Jérôme Torrisani, Bushra Ateq, Alexander Unterberger, Patrick Salamé, Sebastian Alvarado, Jing-Ni Ou, Catalina D'Allessio, Nadine Provençal, Sachin Tendulakar, Marilyne Blain, Joanne Wyglinski, Shaffat Rabbani, Moshe Szyf

Bibliographic record

VenueCancer Research · 2008
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicEpigenetics and DNA Methylation
Canadian institutionsMcGill University
Fundersnot available
KeywordsCancer researchDNA methylationBiologyDemethylating agentEctopic expressionDNA demethylationCarcinogenesisCell cultureCancerCancer cellGene knockdownMetastasisMolecular biologyGene expressionGeneGenetics
DOInot available

Abstract

fetched live from OpenAlex

13 Introduction: Cancer cells are hallmarked by global DNA hypomethylation. MBD2 is the only protein that has been implicated in removal of methyl groups from CG di-nucleotides. Inhibition of MBD2 attenuates tumorigenesis, metastasis, and reverses the hypomethylation of metastatic genes. Additionally, germ line deletion of the mbd2 gene protects mice from intestinal tumors; therefore, we tested the hypothesis that oncogenic signals induce MBD2 resulting in metastatic transformation of cells through the triggering of global DNA hypomethylation resulting in metastatic gene activation.
 Results: Ectopic MBD2 expression but not mutant MBD2 causes global genomic demethylation in normal (NIH 3T3, MCF10A, Primary Human Fibroblasts, and Primary Hepatocytes) and transformed (MCF7, HA-RAS-NIH3T3, and T24) cell lines. MBD2 knockdown in these cell lines results in increased DNA methylation supporting the hypothesis that MBD2 is involved in global hypomethylation. Furthermore, cell lines with increased MBD2 have greater in-vitro demethylase activity. Ectopic MBD2 causes normal cells to become highly transformed and invasive and increases the invasiveness of transformed cell lines. MBD2 overexpressing cells are tumorgenic in NUDE mice and invade and degrade the bone of SCID mice. We show that MBD2 causes this by binding to and demethylating the gene promoters of cell type specific gene sets. We have identified several metastatic promoting genes like MerTK as well as novel metastatic genes that are regulated by MBD2 promoted demethylation. We have proven that these genes are required for metastasis using siRNA strategies in transformed cell lines and developed a therapeutic intervention strategy against a novel metastatic target. Finally, we show that MBD2 is induced by activated HA-RAS, regulates demethylation and metastatic gene activation in these cells, and is regulated by HA-RAS associated transcription factors.
 Summary: Our results have unraveled a critical transformation pathway leading from RAS through MBD2 to global hypomethylation and activation of metastatic genes as well. These data support a new therapeutic approach to metastasis, which would involve targeting MBD2 and DNA demethylation.
 Supported by a grant from the National Cancer Institute of Canada to MS.

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 score0.001
Threshold uncertainty score0.005

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 integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

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 head0.079
GPT teacher head0.358
Teacher spread0.279 · 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".

Quick stats

Citations2
Published2008
Admission routes2
Has abstractyes

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