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  • Open Access

    ARTICLE

    miR 204-5p inhibits apoptosis in dacarbazine-treated melanoma cells

    NADEZHDA PALKINA, EKATERINA SERGEEVA, TATIANA RUKSHA*

    Oncology Research, Vol.29, No.6, pp. 393-400, 2021, DOI:10.32604/or.2022.025816 - 10 November 2022

    Abstract Melanoma is one of the most aggressive types of malignant tumors, commonly affecting young individuals. The treatment of metastatic tumors remains obscure due to the resistance of tumor cells to drugs mediated by various mechanisms. The acquisition of a resistant phenotype is associated with both genetic and epigenetic alterations in cancer cells. Therefore, the current study aimed to investigate whether microRNA (miR)-204-5p could promote alterations in the cell cycle and apoptosis of dacarbazine (DTIC)-treated melanoma cells. Quantitative real time PCR showed that transfection of DTIC-treated SK-MEL-2 melanoma cells with miR-204-5p mimics significantly upregulated miR-204-5p. However,… More >

  • Open Access

    ARTICLE

    Examining the In Vitro Efficacy of the IAP Antagonist Birinapant as a Single Agent or in Combination With Dacarbazine to Induce Melanoma Cell Death

    Vesna Vetma*†‡, Jan Rožanc§, Emilie M. Charles*†, Christian T. Hellwig*†‡¶, Leonidas G. Alexopoulos§#, Markus Rehm*†‡#

    Oncology Research, Vol.25, No.9, pp. 1489-1494, 2017, DOI:10.3727/096504017X14897145996933

    Abstract Antagonists of inhibitors of apoptosis proteins (IAPs), alone or in combination with genotoxic therapeutics, have been shown to efficiently induce cell death in various solid tumors. The IAP antagonist birinapant is currently being tested in phase II clinical trials. We herein aimed to investigate the antitumor efficacy of dacarbazine in vitro, both as a single agent and in combination with birinapant, in melanoma cell lines. Covering clinically relevant drug concentration ranges, we conducted a total of 5,400 measurements in a panel of 12 human melanoma cell lines representing different stages of disease progression. Surprisingly, functionally More >

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