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Record W2967020362

Role of non-mutational mechanisms in cancer cell drug resistance

2008· article· en· W2967020362 on OpenAlexaff
В Ф Чехун, Jody Filkowski, James Meservy, Yaroslav Ilnytskyy, Dmytro Mykytenko, Volodymyr Tryndyak, Igor P. Pogribny, Olga Kovalchuk

Bibliographic record

VenueCancer Research · 2008
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicKruppel-like factors research
Canadian institutionsUniversity of Lethbridge
Fundersnot available
KeywordsBiologyCancer researchCancerCancer cellBreast cancerDNA methylationEstrogen receptorGeneticsGeneGene expression
DOInot available

Abstract

fetched live from OpenAlex

3211 Many chemotherapy regiments are used effectively to treat breast cancer; however, breast cancer cells often become resistant to the drugs, which usually leads to a relapse and worsening of prognosis. The acquisition of drug resistance is a major clinical obstacle to the successful treatment of breast cancer. The causes of cancer-specific drug resistance are currently believed to be linked to: (i) random drug-induced mutational events (genetic hypothesis), (ii) drug-induced non-mutational alterations of gene function (epigenetic hypothesis), and/or (iii) drug-induced karyotypic changes (karyotypic hypothesis). In the present study, we examined the role of non-mutational mechanisms in the development of a multidrug-resistant phenotype of MCF-7 human breast cancer cells induced by doxorubicin (DOX) and cisplatin (cisDDP), two chemotherapeutic drugs with different modes of action. Both of the drug-resistant cell lines were characterized by extensive alterations in gene-specific cytosine methylation, as indicated by the appearance of a number of differentially methylated DNA genes. A detailed analysis of hypo- and hypermethylated DNA sequences revealed that in addition to specific alterations induced by each of the drugs, the acquisition of the drug-resistant phenotype of MCF-7 cells to DOX and cisDDP was characterized by three common features: dysfunction of genes involved in estrogen metabolism (sulfatase 2 and estrogen receptor α), apoptosis (p53, p73, α-tubulin, BCL2-antagonist of cell death, tissue transglutaminase 2, and forkhead box protein K1), and cell-cell contact (leptin, stromal cell derived factor receptor 1, activin A receptor, and E-cadherin). The analysis also showed that two opposing hypo- and hypermethylation processes may enhance and complement each other in the disruption of these pathways.
 Another non-mutational mechanism of gene expression control is mediated via the function of small regulatory RNAs, particularly microRNAs (miRNAs). How these miRNAs might be involved in cancer cell drug resistance remains largely unexplored. MCF-7/DOX cells exhibited a considerable dysregulation of the miRNAome profile. In addition, miR-451 was found to regulate the expression of the multidrug resistance 1 (mdr1) gene. More importantly, transfection of the MCF-7/DOX resistant cells with miR-451 resulted in an increased sensitivity of cells to DOX. These results provide evidence that non-mutational mechanisms are an important feature of cancer cells with the acquired drug-resistant phenotype and may be a crucial contributing factor to its development. Furthermore, the potential reversibility of these alterations may have significant implications for novel therapeutic strategies to overcome cancer cell resistance.

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 score0.006
Threshold uncertainty score0.568

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 head0.031
GPT teacher head0.372
Teacher spread0.341 · 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
Published2008
Admission routes1
Has abstractyes

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