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Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
Gal-3 does not suppress cisplatin-induced apoptosis in A-375 melanoma cells
Małgorzata Pokrywka1,2, Monika Bubka3, Marcelina Janik3
1Chair of Clinical Biochemistry, Jagiellonian University Medical College, Kopernika 15A, 31-501 Kraków, Poland.
Abstract:
Melanoma is the most aggressive of all skin cancers and is exceptionally resistant to therapies. During melanoma progression, cancer cells reprogram their proliferation and survival pathways and achieve resistance to treatment-induced apoptosis. Galectin-3 (gal-3) is a member of the lectin family and is involved in such biological processes as cell adhesion, growth and differentiation, the cell cycle, and apoptosis. Gal-3 also plays an important role in tumor development and metastasis. The relationship between gal-3 expression and these processes is specific to the tumor type and the stage of cancer progression. The biological functions of gal-3 depend on its localization in the cell. In the present study, human metastatic melanoma A-375 cells, characterized by weak endogenous expression of gal-3, were transfected with gal-3 cDNA and cisplatin-induced apoptosis was measured. Data from AnnexinV and mitochondrial membrane potential analysis revealed that gal-3 did not protect the A-375 melanoma cells against cisplatin. This result probably is associated with its nuclear localization in the cells.
Insights
Galectin-3 (gal-3) did not protect metastatic melanoma cells from cisplatin-induced apoptosis. Nuclear localization of gal-3 in these cells may explain its lack of protective effect against chemotherapy.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Melanoma is an aggressive skin cancer known for therapy resistance.
- Cancer cells alter proliferation and survival pathways, resisting apoptosis during progression.
- Galectin-3 (gal-3) influences cell adhesion, growth, cell cycle, apoptosis, and metastasis.
Purpose of the Study:
- To investigate the role of galectin-3 (gal-3) in cisplatin-induced apoptosis in human metastatic melanoma cells.
- To determine if gal-3 expression influences melanoma cell survival under chemotherapeutic stress.
Main Methods:
- Human metastatic melanoma A-375 cells with low endogenous gal-3 were transfected with gal-3 cDNA.
- Cisplatin-induced apoptosis was measured using Annexin V staining and mitochondrial membrane potential analysis.
Main Results:
- Galectin-3 (gal-3) expression did not confer protection to A-375 melanoma cells against cisplatin treatment.
- Annexin V and mitochondrial potential data indicated no significant anti-apoptotic effect of gal-3.
Conclusions:
- Galectin-3 (gal-3) does not protect against cisplatin-induced apoptosis in this melanoma model.
- The nuclear localization of gal-3 in A-375 cells may account for its failure to protect against chemotherapy.
