Now showing items 1-5 of 5
Polyamines modulate the roscovitine-induced cell death switch decision autophagy vs. apoptosis in MCF-7 and MDA-MB-231 breast cancer cells
(Spandidos Publ Ltd, Pob 18179, Athens, 116 10, Greece, 2015-06)
Current clinical strategies against breast cancer mainly involve the use of anti-hormonal agents to decrease estrogen production; however, development of resistance is a major problem. The resistance phenotype depends on ...
CDK inhibitors-induced SSAT expression requires NF kappa B and PPAR gamma in MCF-7 breast cancer cells
(TUBİTAK Scientific & Technical Research Council Turkey, Ataturk Bulvarı No 221, Kavaklıdere, Ankara, 00000, Turkey, 2015)
The cyclin-dependent kinase (CDK) inhibitors purvalanol and roscovitine are therapeutic agents that control cell proliferation through regulating cell-cycle machinery. They also affect polyamine (PA) metabolism, which is ...
Cyclin-dependent kinase inhibitors, roscovitine and purvalanol, induce apoptosis and autophagy related to unfolded protein response in HeLa cervical cancer cells
(Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands, 2018-10)
Roscovitine (Rosc) and purvalanol (Pur) are competitive inhibitors of cyclin-dependent kinases (CDKs) by targeting their ATP-binding pockets. Both drugs are shown to be effective to decrease cell viability and dysregulate ...
Roscovitine-treated He La cells finalize autophagy later than apoptosis by downregulating Bcl-2
(Spandidos Publ Ltd, Pob 18179, Athens, 116 10, Greece, 2015-03)
The cell cycle is tightly regulated by the family of cyclin-dependent kinases (CDKs). CDKs act as regulatory factors on serine and threonine residues by phosphorylating their substrates and cyclins. CDK-targeting drugs ...
mTOR is a fine tuning molecule in CDK inhibitors-induced distinct cell death mechanisms via PI3K/AKT/mTOR signaling axis in prostate cancer cells
(Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands, 2016-10)
Purvalanol and roscovitine are cyclin dependent kinase (CDK) inhibitors that induce cell cycle arrest and apoptosis in various cancer cells. We further hypothesized that co-treatment of CDK inhibitors with rapamycin, an ...