Phenotypical alterations induced by glucocorticoids resistance in RPMI 8226 human myeloma cells
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Published on: February 21, 2018
Vincent Genty1, Gérard Dine, Jean Dufer
1Institut Biotechnologique de Troyes, 11 rue Marie Curie, 10000 Troyes, France. v.genty.ibt@wanadoo.fr
Abstract:
Resistance to glucocorticoids (GCs) frequently appears during treatment of hematological malignancies. This study investigates the phenotypical alterations observed in human myeloma cell sublines resistant to glucocorticoids. Using the RPMI8226 cell line, the cytotoxic efficiencies of four glucocorticoids, and the phenotypes of isolated resistant sublines were analyzed. Methyl-prednisolone and dexamethasone exhibited the higher toxic effects on RPMI8226 cells. All corticoids were able to induce drug-resistance. Resistant sublines showed an increased expression of the alpha-isoform of the glucocorticoid receptors (GRs), and specific modulations in CD23, CD38, CD44 and CD58 expressions. Thus, glucocorticoid resistance in RPMI8226 cells is accompanied by significant phenotypical alterations that could be implicated in survival enhancement to therapy and/or tumor spreading.
Insights
Glucocorticoid resistance in myeloma cells involves changes in cell surface markers and increased glucocorticoid receptors (GRs). These alterations may enhance cancer cell survival and spread during therapy.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- Glucocorticoids (GCs) are crucial in treating hematological malignancies.
- Acquired resistance to GCs is a significant clinical challenge in these cancers.
Purpose of the Study:
- To investigate phenotypical changes in human myeloma cell sublines resistant to glucocorticoids.
- To analyze the cytotoxic effects of various GCs and characterize resistant cell phenotypes.
Main Methods:
- Utilized the RPMI8226 human myeloma cell line.
- Assessed cytotoxic efficiencies of four different glucocorticoids.
- Isolated and analyzed phenotypes of resistant sublines, including receptor expression and cell surface marker modulation.
Main Results:
- Methylprednisolone and dexamethasone showed the highest cytotoxicity against RPMI8226 cells.
- All tested glucocorticoids induced drug resistance.
- Resistant sublines exhibited increased alpha-isoform glucocorticoid receptor (GR) expression.
- Specific modulations were observed in CD23, CD38, CD44, and CD58 expressions.
Conclusions:
- Glucocorticoid resistance in RPMI8226 myeloma cells is associated with significant phenotypical alterations.
- These alterations, including GR upregulation and changes in cell surface markers, may contribute to enhanced therapeutic survival and tumor dissemination.
