Transcriptomic Changes in Cisplatin-Resistant MCF-7 Cells.

MCF-7 cells RNAs breast cancer cisplatin resistance transcriptome vesicles

Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
29 Mar 2024
Historique:
received: 12 10 2023
revised: 13 02 2024
accepted: 23 02 2024
medline: 13 4 2024
pubmed: 13 4 2024
entrez: 13 4 2024
Statut: epublish

Résumé

Breast cancer is a leading cause of cancer-related deaths among women. Cisplatin is used for treatment, but the development of resistance in cancer cells is a significant concern. This study aimed to investigate changes in the transcriptomes of cisplatin-resistant MCF7 cells. We conducted RNA sequencing of cisplatin-resistant MCF7 cells, followed by differential expression analysis and bioinformatic investigations to identify changes in gene expression and modified signal transduction pathways. We examined the size and quantity of extracellular vesicles. A total of 724 genes exhibited differential expression, predominantly consisting of protein-coding RNAs. Notably, two long non-coding RNAs (lncRNAs), NEAT1 and MALAT, were found to be dysregulated. Bioinformatic analysis unveiled dysregulation in processes related to DNA synthesis and repair, cell cycle regulation, immune response, and cellular communication. Additionally, modifications were observed in events associated with extracellular vesicles. Conditioned media from resistant cells conferred resistance to wild-type cells in vitro. Furthermore, there was an increase in the number of vesicles in cisplatin-resistant cells. Cisplatin-resistant MCF7 cells displayed differential RNA expression, including the dysregulation of NEAT1 and MALAT long non-coding RNAs. Key processes related to DNA and extracellular vesicles were found to be altered. The increased number of extracellular vesicles in resistant cells may contribute to acquired resistance in wild-type cells.

Identifiants

pubmed: 38612643
pii: ijms25073820
doi: 10.3390/ijms25073820
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Consejo Nacional de Humanidades, Ciencias y Tecnologías
ID : 902712

Auteurs

Araceli Ruiz-Silvestre (A)

Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.
Posgrado en Ciencias Biomédicas, Universidad Nacional Autónoma de Mexico (UNAM), Ciudad de Mexico 04510, Mexico.

Alfredo Garcia-Venzor (A)

Department of Life Sciences, Ben-Gurion University of the Negev, Beer Sheva 8410501, Israel.

Gisela Ceballos-Cancino (G)

Laboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

José M Sánchez-López (JM)

Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

Karla Vazquez-Santillan (K)

Laboratorio de Innovación en Medicina de Precisión, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

Gretel Mendoza-Almanza (G)

Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.
Consejo Nacional de Ciencia y Tecnologia, Ciudad de Mexico 03940, Mexico.

Floria Lizarraga (F)

Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

Jorge Melendez-Zajgla (J)

Laboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

Vilma Maldonado (V)

Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

Classifications MeSH