E2F1-mediated DNA damage is implicated in 8-Cl-adenosine-induced chromosome missegregation and apoptosis in human lung cancer H1299 cells

[1]  I. Talianidis,et al.  Lysine methylation regulates E2F1-induced cell death. , 2010, Molecular cell.

[2]  M. Inagaki,et al.  DNA Lesions Induced by Replication Stress Trigger Mitotic Aberration and Tetraploidy Development , 2010, PloS one.

[3]  I. Bossis,et al.  8-Cl-adenosine inhibits proliferation and causes apoptosis in B-lymphocytes via protein kinase A-dependent and independent effects: implications for treatment of Carney complex-associated tumors. , 2009, The Journal of clinical endocrinology and metabolism.

[4]  Shuxing Zhang,et al.  Inhibition of ATP synthase by chlorinated adenosine analogue. , 2009, Biochemical pharmacology.

[5]  J. Bartek,et al.  Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas. , 2009, The American journal of pathology.

[6]  M. Piris,et al.  E2F1 expression is deregulated and plays an oncogenic role in sporadic Burkitt's lymphoma. , 2009, Cancer research.

[7]  H. Jia,et al.  Inhibition of CHK1 kinase by Gö6976 converts 8-chloro-adenosine-induced G2/M arrest into S arrest in human myelocytic leukemia K562 cells. , 2009, Biochemical pharmacology.

[8]  H. Jia,et al.  8‐chloro‐adenosine‐induced E2F1 promotes p14ARF gene activation in H1299 cells through displacing Sp1 from multiple overlapping E2F1/Sp1 sites , 2009, Journal of cellular biochemistry.

[9]  H. Jia,et al.  Inhibition of topoisomerase II by 8-chloro-adenosine triphosphate induces DNA double-stranded breaks in 8-chloro-adenosine-exposed human myelocytic leukemia K562 cells. , 2009, Biochemical pharmacology.

[10]  C. Stratakis,et al.  Protein kinase A-independent inhibition of proliferation and induction of apoptosis in human thyroid cancer cells by 8-Cl-adenosine. , 2008, The Journal of clinical endocrinology and metabolism.

[11]  K. Fukasawa.  Oncogenes and tumour suppressors take on centrosomes , 2007, Nature Reviews Cancer.

[12]  E. Knudsen,et al.  RB Loss Promotes Aberrant Ploidy by Deregulating Levels and Activity of DNA Replication Factors* , 2007, Journal of Biological Chemistry.

[13]  R. Macklis,et al.  E2F4 regulates a stable G2 arrest response to genotoxic stress in prostate carcinoma , 2007, Oncogene.

[14]  P. Jeggo,et al.  Chromosome breakage after G2 checkpoint release , 2007, The Journal of cell biology.

[15]  H. Jia,et al.  8-Chloro-adenosine inhibits growth at least partly by interfering with actin polymerization in cultured human lung cancer cells. , 2006, Biochemical pharmacology.

[16]  D. Banerjee,et al.  E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents. , 2006, Cancer research.

[17]  M. Pickering,et al.  Rb inactivation leads to E2F1-mediated DNA double-strand break accumulation , 2006, Oncogene.

[18]  V. Gorgoulis,et al.  Involvement of E2F transcription factor family in cancer. , 2005, European journal of cancer.

[19]  Y. Ahn,et al.  8-Chloro-cyclic AMP-induced growth inhibition and apoptosis is mediated by p38 mitogen-activated protein kinase activation in HL60 cells. , 2005, Cancer research.

[20]  M. Keating,et al.  Cell death of bioenergetically compromised and transcriptionally challenged CLL lymphocytes by chlorinated ATP. , 2005, Blood.

[21]  I. Lossos,et al.  Apoptosis-stimulating protein of p53-2 (ASPP2/53BP2L) is an E2F target gene , 2005, Cell Death and Differentiation.

[22]  Hong-Yu Zhang,et al.  Exposure of human lung cancer cells to 8-chloro-adenosine induces G2/M arrest and mitotic catastrophe. , 2004, Neoplasia.

[23]  W. Gerald,et al.  Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control , 2004, Nature.

[24]  Takayuki Nojima,et al.  Induction of Centrosome Amplification and Chromosome Instability in Human Bladder Cancer Cells by p53 Mutation and Cyclin E Overexpression , 2004, Cancer Research.

[25]  Guido Kroemer,et al.  Cell death by mitotic catastrophe: a molecular definition , 2004, Oncogene.

[26]  C. M. Stellrecht,et al.  RNA-directed actions of 8-chloro-adenosine in multiple myeloma cells. , 2003, Cancer research.

[27]  J. Nevins,et al.  Specificity in the activation and control of transcription factor E2F-dependent apoptosis , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[28]  I. Screpanti,et al.  Differential regulation of E2F1 apoptotic target genes in response to DNA damage , 2003, Nature Cell Biology.

[29]  C. Stevens,et al.  Chk2 activates E2F-1 in response to DNA damage , 2003, Nature Cell Biology.

[30]  Y. Kalma,et al.  E2Fs up-regulate expression of genes involved in DNA replication, DNA repair and mitosis , 2002, Oncogene.

[31]  L. Rakić,et al.  8-Cl-cAMP Affects Glioma Cell-Cycle Kinetics and Selectively Induces Apoptosis , 2002, Cancer investigation.

[32]  A. Harris,et al.  8-Cl-adenosine is an active metabolite of 8-Cl-cAMP responsible for its in vitro antiproliferative effects on CHO mutants hypersensitive to cytostatic drugs , 2001, Cancer Chemotherapy and Pharmacology.

[33]  I. Roninson,et al.  If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells. , 2001, Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy.

[34]  V. Gandhi,et al.  8-chloro-cAMP and 8-chloro-adenosine act by the same mechanism in multiple myeloma cells. , 2001, Cancer research.

[35]  J. Nevins,et al.  Selective induction of E2F1 in response to DNA damage, mediated by ATM-dependent phosphorylation. , 2001, Genes & development.

[36]  Sang Gyun Kim,et al.  8‐Cl‐cAMP induces cell cycle‐specific apoptosis in human cancer cells , 2001, International journal of cancer.

[37]  R. Chinery,et al.  8-Cl-adenosine-induced inhibition of colorectal cancer growth in vitro and in vivo. , 2000, Neoplasia.

[38]  Y. Cho‐Chung,et al.  Dual anticancer activity of 8-Cl-cAMP: inhibition of cell proliferation and induction of apoptotic cell death. , 2000, Biochemical and biophysical research communications.

[39]  C. Blattner,et al.  Transcription Factor E2F-1 Is Upregulated in Response to DNA Damage in a Manner Analogous to That of p53 , 1999, Molecular and Cellular Biology.

[40]  M. Scheffner,et al.  Interaction between ubiquitin–protein ligase SCFSKP2 and E2F-1 underlies the regulation of E2F-1 degradation , 1999, Nature Cell Biology.

[41]  N. Krett,et al.  8Cl-cAMP Cytotoxicity in Both Steroid Sensitive and Insensitive Multiple Myeloma Cell Lines Is Mediated by 8Cl-Adenosine , 1998 .

[42]  Y. Cho‐Chung,et al.  8-chloroadenosine 3',5'-monophosphate (8-Cl-cAMP) selectively eliminates protein kinase A type I to induce growth inhibition in c-ras-transformed fibroblasts. , 1998, European journal of cancer.

[43]  C. Allis,et al.  Mitosis-specific phosphorylation of histone H3 initiates primarily within pericentromeric heterochromatin during G2 and spreads in an ordered fashion coincident with mitotic chromosome condensation , 1997, Chromosoma.

[44]  D. Noonan,et al.  The cAMP analog 8‐Cl‐cAMP inhibits growth and induces differentiation and apoptosis in retinoblastoma cells , 1997 .

[45]  J. Bartek,et al.  Deregulated expression of E2F family members induces S-phase entry and overcomes p16INK4A-mediated growth suppression , 1996, Molecular and cellular biology.

[46]  J. Nevins,et al.  Expression of transcription factor E2F1 induces quiescent cells to enter S phase , 1993, Nature.

[47]  J. C. Stoof,et al.  Growth inhibition of human glioma cells induced by 8-chloroadenosine, an active metabolite of 8-chloro cyclic adenosine 3':5'-monophosphate. , 1992, Cancer research.