Vemurafenib-induced Increase in Ki-67-Negative Cells in BRAF-Negative Melanoma

Vemurafenib revolutionized the treatment of melanomas which harbor mutations in BRAF oncogene whereas BRAF -negative tumors are resistant to its antitumor effects. Meanwhile tumor chemoresistance is associated with the presence of quiescent, resting-dormant (G 0 -positive, Ki-67-negative) cancer cel...

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Bibliographic Details
Published in:Cell and tissue biology 2021-05, Vol.15 (3), p.227-235
Main Authors: Nikolaeva, E. D., Dubovtseva, I. Yu, Belonogov, R. N., Narkevich, A. N., Moshev, A. V., Savchenko, A. A., Ruksha, T. G.
Format: Article
Language:English
Subjects:
Antitumor activity
Biomedical and Life Sciences
Cell Biology
Cell cycle
Chemoresistance
Cyclin-dependent kinase 4
Gene expression
Life Sciences
Melanoma
Regulatory proteins
Tumors
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Summary:Vemurafenib revolutionized the treatment of melanomas which harbor mutations in BRAF oncogene whereas BRAF -negative tumors are resistant to its antitumor effects. Meanwhile tumor chemoresistance is associated with the presence of quiescent, resting-dormant (G 0 -positive, Ki-67-negative) cancer cells in the heterogeneous cancer cell population. In order to test if BRAF-inhibitor can stimulate quiescence in melanoma cells, two melanoma cell lines (BRO and SK-MEL-2) were treated with the antitumor drug vemurafenib, and populations with G 1 /G 0 cell cycle arrest were obtained. The latter were confirmed by negative staining with Ki-67 antibodies, and changes in the gene expression of cell cycle regulatory proteins, such as CDK4 , CCND1 and CDKN1B .
ISSN:1990-519X
1990-5203
DOI:10.1134/S1990519X2103007X