Material and Methods: Cyclin D, E, A, and B, and cyclin-dependent kinase inhibitor (CDK1) p16 and p21 levels were measured via flow cytometry in patients with chronic myeloid leukemia (CML) (n = 16) and multiple myeloma (MM) (n = 13), and in controls (n = 15).
Among all the cyclins expressed during the S phase, cyclin D expression was the lowest in the CML patients.
Although myeloma tumors exhibit complex karyotypes, and a variety of structural and quantitative chromosomal abnormalities, these tumors are unified in their ubiquitous targeting of cyclin D genes for overexpression (14).
Comparison of the cell cycle-regulating elements cyclin A, B, D, and E, and CDKIs p16 and p21 in the control group showed that cyclin D was expressed most frequently during the GO/G1 phase; the other cyclins were present in 33% of the cells, and the cyclin E level was very low.
Cyclin D had the lowest level of expression of all the cyclins during the S phase, unlike in the control group (P < 0.
Table 4: Percentage of Cells Expressing Cyclins and CDKIs, According to Phase G0/G1 Cyclin A Cyclin B Cyclin D Cyclin E p21 p16 CML 26 21.
When passing through the R checkpoint cyclin type D is expressed (23); thus, the expression of cyclin D as the major cyclin occurs during the GO/G1 phase (24).
Daidzein treatment resulted in decreases in cyclin D, CDK2, and CDK4, whereas the expression of CDK6 and cyclin E was unchanged.
Antibodies against CDK1, CDK2, CDK4, cyclin A, cyclin B, cyclin D, cyclin E, p[21.
In MCF-7 cells, daidzein decreased cyclin D expression by 28.
G1-phase progression and G1/S-phase transition are regulated by CDK2 and CDK4, which assemble with cyclin E and cyclin D.