N6-Isopentenyladenosine and its Analogue N6-Benzyladenosine Induce Cell Cycle Arrest and Apoptosis in Bladder

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)

Volume 15, 10 Issues, 2015

Download PDF Flyer

Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 22nd of 58 in Chemistry, Medicinal
  • 85th of 202 in Oncology

Submit Abstracts Online Submit Manuscripts Online

Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 2.939
5 - Year: 3.37

N6-Isopentenyladenosine and its Analogue N6-Benzyladenosine Induce Cell Cycle Arrest and Apoptosis in Bladder

Author(s): Sara Castiglioni, Silvana Casati, Roberta Ottria, Pierangela Ciuffreda and Jeanette A. M. Maier


Cytokinins are phytohormones critically involved in the regulation of plant growth and development. They also affect the proliferation and differentiation of animal cells, thus representing new tools to treat diseases that involve dysfunctional cell growth and/or differentiation. Recently, by performing structure-function studies on human cells, we found that only N6-isopentenyladenosine and its benzyl analogue N6-benzyladenosine suppress the clonogenic activity and the growth of different neoplastic cells. We here broaden our studies on bladder carcinoma T24 cells, because, due to the high recurrence rate of bladder cancer, new active molecules are sought to contrast the growth of this tumor. Early events induced by N6-isopentenyladenosine and N6-benzyladenosine are the alteration of T24 cell morphology and the disorganization of the actin cytoskeleton. After 24 h N6-isopentenyladenosine and N6-benzyladenosine inhibit growth by arresting the cells in the G0/G1 phase of the cell cycle. We also show that the two compounds induce apoptosis, an event linked to the activation of caspase 3. Since DNA damage is a prime factor resulting in cell cycle arrest and apoptosis, it is noteworthy that we do not detect any genotoxic effect upon treatment of T24 cells with N6-isopentenyladenosine and N6- benzyladenosine.

Because the disruption of actin filaments leads to G1 arrest and is also implicated in apoptosis, we hypothesize that cytoskeletal rearrangement might be responsible for triggering the antiproliferative and proapotpotic effects of N6-isopentenyladenosine and N6-benzyladenosine in T24 cells.

Purchase Online Order Reprints Order Eprints Rights and Permissions


Article Details

Volume: 13
First Page:
Page Count:
DOI: 10.2174/1871520613666131125144105

Webmaster Contact: urooj@benthamscience.org Copyright © 2015 Bentham Science