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In contrast, STMpc cells induced to express SMARCB1 showed little change in the cell cycle (Supplementary Figure S1A).
NOM alone failed to induce any change in the cell cycle (Fig. 7 and Table 4).
However, curcumin treatment did not cause any change in the cell cycle distribution of normal HPDE-6 cells.
However, we observed an upregulation of DR4 and LRDD, both p53-induced pro-apoptotic genes, with no change in the cell cycle arrest-related gene, p21.
Since levels of Skp1 do not change in the cell cycle, this protein served as an internal control to normalize for loading of cellular protein.
Whole mount antibody staining for an accepted proliferation marker, phospho-histone H3 (pH3) shows that there is no visible change in the cell cycle in enosf1b-knockdown embryos.
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The changes in the cell cycle distribution are associated with changed expression levels of CDKN1B (p27Kip1), a general inhibitor of Cyclin-CDK complexes and, thereby, of cell cycle progression.
However, no significant changes in the cell cycle patterns were observed between untransfected and Sin3B transfected cells under normal cycling conditions/without drug treatment.
This instability may be related to changes in the cell cycle and extracellular matrix degradation.
In addition, knockdown of MELK with siRNA decreased cell proliferation and caused changes in the cell cycle after radiation or 5-FU treatment.
Regarding the mechanistic aspects of the above cytotoxic activity, flow cytometric analysis of DNA content did not reveal significant changes in the cell cycle phase distribution of rhodanine-treated HT-1080 comparedmpared with control ones, with the exception of an S-phase arrest caused by compounds 43 and 45 at 48 h (not shown).
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