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


Krasnoyarsk State Medical University, Krasnoyarsk, 660022, Russian Federation

* Corresponding Author: TATIANA RUKSHA. Email:

Oncology Research 2021, 29(6), 393-400.


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, flow cytometric analysis revealed that the proportion of cells in different phases of the cell cycle remained unchanged. Additionally, the proportion of early apoptotic cells was notably enhanced following cell treatment with DTIC, accompanied by a profound increase in Ki-67 negative cells, as verified by an immunofluorescence assay. Furthermore, miR-204-5p overexpression reduced the percentage of early apoptotic DTIC-treated melanoma cells. The proportion of Ki-67 negative cells was only increased by 3%. Overall, the results of the current study indicated that miR-204-5p overexpression could mostly attenuate cell apoptosis in DTIC-treated cells rather than promote their transition from the G0 phase of the cell cycle in response to chemotherapeutic agent-induced stress.


Cite This Article

PALKINA, N., SERGEEVA, E., RUKSHA, T. (2021). miR 204-5p inhibits apoptosis in dacarbazine-treated melanoma cells. Oncology Research, 29(6), 393–400.

This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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