Transcriptomic Changes in Cisplatin-Resistant MCF-7 Cells.
Araceli Ruiz-SilvestreAlfredo Garcia-VenzorGisela Ceballos-CancinoJosé M Sánchez-LópezKarla Vazquez-SantillanGretel Mendoza-AlmanzaFloria LizarragaJorge Melendez-ZajglaVilma Maldonado-LagunasPublished in: International journal of molecular sciences (2024)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- gene expression
- cell cycle
- immune response
- endoplasmic reticulum stress
- type diabetes
- metabolic syndrome
- poor prognosis
- wild type
- single cell
- skeletal muscle
- genome wide
- young adults
- dendritic cells
- insulin resistance
- transcription factor
- combination therapy
- replacement therapy
- drug induced