Evidence map›Paper›PMID 39034849›Full record

ArticleBioscience reports2024

Tamoxifen metabolites treatment promotes ERα+ transition to triple negative phenotype in vitro, effects of LDL in chemoresistance.

Andrea Muñoz-Ayala, Brenda Chimal-Vega, Nicolás Serafín-Higuera, Octavio Galindo-Hernández, Gladys Ramírez-Rosales, Iván Córdova-Guerrero, Luis Fernando Gómez-Lucas, Victor García-González

Abstract read
In one paragraph

Article in Bioscience reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Andrea Muñoz-AyalaDepartamento de Bioquímica, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Brenda Chimal-VegaDepartamento de Bioquímica, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Nicolás Serafín-HigueraFacultad de Odontología Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Octavio Galindo-HernándezDepartamento de Bioquímica, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Gladys Ramírez-RosalesDepartamento de Inmunología, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Iván Córdova-GuerreroFacultad de Ciencias Químicas e Ingeniería, Universidad Autónoma de Baja California, Tijuana 22390, México.
Luis Fernando Gómez-LucasDepartamento de Bioquímica, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.
Victor García-GonzálezDepartamento de Bioquímica, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Mexicali 21000, México.ORCID 0009-0007-2715-9811

Funding

Consejo Nacional de Ciencia y Tecnología (CONACYT) A1-S-28653/SEP/CONACYTUniversidad Autónoma de Baja California (AUBC) 2-12-213-2-003-2-1994. 23a. Convocatoria Interna de Apoyo a Proyectos de Investigación
6 · The paper itself

Abstract

objectiveEstrogen receptor-positive (ER+) breast cancer represents about 80% of cases, tamoxifen is the election neoadjuvant chemotherapy. However, a large percentage of patients develop chemoresistance, compromising recovery. Clinical evidence suggests that high plasmatic levels of low-density lipoproteins (LDL) could promote cancer progression. The present study analyzed the effect of LDL on the primary plasmatic active Tamoxifen's metabolites resistance acquisition, 4-hydroxytamoxifen (4OH-Tam) and 4-hydroxy-N-desmethyl-tamoxifen (endoxifen), in breast cancer ERα + cells (MCF-7).

methodsTwo resistant cellular variants, MCF-7Var-H and MCF-7Var-I, were generated by a novel strategy and their phenotype features were evaluated. Phenotypic assessment was performed by MTT assays, cytometry, immunofluorescence microscopy, zymography and protein expression analysis.

resultsMCF-7Var-H, generated only with tamoxifen metabolites, showed a critical down-regulation in hormone receptors, augmented migration capacity, metalloprotease 9 extracellular medium excretion, and a mesenchymal morphology in contrast with native MCF-7, suggesting the transition towards Triple-negative breast cancer (TNBC) phenotype. In contrast, MCF-7Var-I which was generated in a high LDL media, showed only a slight upregulation in ER and other less noticeable metabolic adaptations. Results suggest a potential role of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) in phenotypic differences observed among variants.

conclusionLDL high or low concentrations during Tamoxifen´s metabolites chemoresistance acquisition leads to different cellular mechanisms related to chemoresistance. A novel adaptative cellular response associated with Nrf2 activity could be implicated.

Indexed as

Drug Resistance, NeoplasmEstrogen Receptor alphaLipoproteins, LDLPhenotypeTamoxifenTriple Negative Breast NeoplasmsAntineoplastic Agents, HormonalBreast NeoplasmsCell MovementFemaleGene Expression Regulation, NeoplasticHumansMCF-7 Cells4-hydroxy-N-desmethyltamoxifenafimoxifeneAntineoplastic Agents, HormonalESR1 protein, humanEstrogen Receptor alphaLipoproteins, LDLTamoxifenbreast cancerschemoresistancemetastasisNrf2tamoxifen

Identifiers

PMID39034849
PMCPMC11301570

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.