Now showing items 1-5 of 5
Epibrassinolide alters PI3K/MAPK signaling axis via activating Foxo3a-induced mitochondria-mediated apoptosis in colon cancer cells
(Elsevier Inc, 525 B Street, Ste 1900, San Diego, Ca 92101-4495 Usa, 2015-10-15)
Epibrassinolide (EBR), a steroid-derived plant growth regulator, has been recently suggested as an apoptotic inducer in different cancer cells. In this experimental study, we investigated the potential apoptotic effect of ...
Purvalanol A is a strong apoptotic inducer via activating polyamine catabolic pathway in MCF-7 estrogen receptor positive breast cancer cells
(Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands, 2014)
Purvalanol A is a specific CDK inhibitor which triggers apoptosis by causing cell cycle arrest in cancer cells. Although it has strong apoptotic potential, the mechanistic action of Purvalanol A on significant cell signaling ...
CDK Inhibitors Induce Mitochondria-mediated Apoptosis Through the Activation of Polyamine Catabolic Pathway in LNCaP, DU145 and PC3 Prostate Cancer Cells
(Bentham Science Publ Ltd, Executive Ste Y-2, Po Box 7917, Saif Zone, 1200 Br Sharjah, U Arab Emirates, 2014-01)
Androgen signaling is critical in prostate cancer development and progression. The co-existence of hormone responsive and irresponsive cells due to functional androgen receptor (AR) in prostate gland is the major obstacle ...
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 ...
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 ...