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...

Full description

Saved in:
Bibliographic Details
Published inCell and tissue biology Vol. 15; no. 3; pp. 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 Journal Article
LanguageEnglish
Published Moscow Pleiades Publishing 01.05.2021
Springer Nature B.V
Subjects
Antitumor activity
Biomedical and Life Sciences
Cell Biology
Cell cycle
Chemoresistance
Cyclin-dependent kinase 4
Gene expression
Life Sciences
Melanoma
Regulatory proteins
Tumors
vemurafenib
Ki-67
melanoma
quiescent cells
cell cycle
G
Online AccessGet full text

Cover

More Information
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