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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
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Transcriptomic Changes in Cisplatin-Resistant MCF-7 Cells.

Araceli Ruiz-Silvestre1,2, Alfredo Garcia-Venzor3, Gisela Ceballos-Cancino4

  • 1Laboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de Mexico 14610, Mexico.

International Journal of Molecular Sciences
|April 13, 2024
PubMed
Summary
This summary is machine-generated.

Cisplatin resistance in breast cancer cells alters gene expression, particularly long non-coding RNAs NEAT1 and MALAT. Increased extracellular vesicles in resistant cells may transfer resistance to other cells.

Keywords:
MCF-7 cellsRNAsbreast cancercisplatinresistancetranscriptomevesicles

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Breast cancer remains a major cause of mortality in women.
  • Cisplatin resistance is a significant challenge in breast cancer treatment.
  • Understanding resistance mechanisms is crucial for improving therapeutic outcomes.

Purpose of the Study:

  • To investigate transcriptomic alterations in cisplatin-resistant MCF7 breast cancer cells.
  • To identify key genes, non-coding RNAs, and pathways involved in cisplatin resistance.
  • To explore the role of extracellular vesicles in the development of cisplatin resistance.

Main Methods:

  • RNA sequencing of cisplatin-resistant MCF7 cells.
  • Differential gene expression analysis and bioinformatic pathway analysis.
  • Examination of extracellular vesicle size and quantity; in vitro resistance transfer assays.

Main Results:

  • 724 genes showed differential expression, including protein-coding RNAs.
  • Two long non-coding RNAs (NEAT1 and MALAT) were significantly dysregulated.
  • Altered pathways included DNA synthesis/repair, cell cycle, immune response, and extracellular vesicle activity.
  • Conditioned media from resistant cells conferred resistance to wild-type cells.
  • Cisplatin-resistant cells exhibited an increased number of extracellular vesicles.

Conclusions:

  • Cisplatin resistance in MCF7 cells is associated with widespread transcriptomic changes, including NEAT1 and MALAT dysregulation.
  • Alterations in DNA-related processes and extracellular vesicle characteristics are key features of resistance.
  • Increased extracellular vesicles in resistant cells may mediate acquired resistance in sensitive cells, suggesting novel therapeutic targets.