CuIIIons and the Stilbene-Chroman Hybrid with a Catechol Moiety Synergistically Induced DNA Damage, and Cell Cycle Arrest and Apoptosis of HepG2 Cells: An Interesting Acid/Base-Promoted Prooxidant Reaction

2012 ◽  
Vol 18 (35) ◽  
pp. 11100-11106 ◽  
Author(s):  
Guo-Yun Liu ◽  
Jie Yang ◽  
Fang Dai ◽  
Wen-Jing Yan ◽  
Qi Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Acid Base ◽  
Cycle Arrest ◽  
Catechol Moiety

ING4 induces G2/M cell cycle arrest and enhances the chemosensitivity to DNA-damage agents in HepG2 cells

FEBS Letters ◽  
2004 ◽  
Vol 570 (1-3) ◽  
pp. 7-12 ◽  
Author(s):  
Xin Zhang ◽  
Lu-Sheng Xu ◽  
Zhi-Qin Wang ◽  
Ke-Sheng Wang ◽  
Na Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
M Cell ◽  
Cycle Arrest

Induction of cell cycle arrest by GL331 via triggering an ATM-dependent DNA damage response in HepG2 cells

2012 ◽  
Vol 14 (7) ◽  
pp. 657-664 ◽  
Author(s):  
Ya-Jie Wang ◽  
Xiao-Guang Chen ◽  
Zhi-Yan Xiao ◽  
Geng-Tao Liu ◽  
Hua Sun
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Dna Damage Response ◽  
Hepg2 Cells ◽  
Cycle Arrest ◽  
Damage Response

scholarly journals Design, Synthesis and Pharmacological Evaluation of Three Novel Dehydroabietyl Piperazine Dithiocarbamate Ruthenium (II) Polypyridyl Complexes as Potential Antitumor Agents: DNA Damage, Cell Cycle Arrest and Apoptosis Induction

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1453
Author(s):  
Haoran Wang ◽  
Jianhua Wei ◽  
Hong Jiang ◽  
Ye Zhang ◽  
Caina Jiang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Antitumor Agents ◽  
Mechanistic Study ◽  
Ros Generation ◽  
Polypyridyl Complexes ◽  
Expression Levels ◽  
Cycle Arrest ◽  
Study Results

The use of cisplatin is severely limited by its toxic side-effects, which has spurred chemists to employ different strategies in the development of new metal-based anticancer agents. Here, three novel dehydroabietyl piperazine dithiocarbamate ruthenium (II) polypyridyl complexes (6a–6c) were synthesized as antitumor agents. Compounds 6a and 6c exhibited better in vitro antiproliferative activity against seven tumor cell lines than cisplatin, they displayed no evident resistance in the cisplatin-resistant cell line A549/DPP. Importantly, 6a effectively inhibited tumor growth in the T-24 xenograft mouse model in comparison with cisplatin. Gel electrophoresis assay indicated that DNA was the potential targets of 6a and 6c, and the upregulation of p-H2AX confirmed this result. Cell cycle arrest studies demonstrated that 6a and 6c arrested the cell cycle at G1 phase, accompanied by the upregulation of the expression levels of the antioncogene p27 and the down-regulation of the expression levels of cyclin E. In addition, 6a and 6c caused the apoptosis of tumor cells along with the upregulation of the expression of Bax, caspase-9, cytochrome c, intracellular Ca2+ release, reactive oxygen species (ROS) generation and the downregulation of Bcl-2. These mechanistic study results suggested that 6a and 6c exerted their antitumor activity by inducing DNA damage, and consequently causing G1 stage arrest and the induction of apoptosis.

scholarly journals ERK activation mediates cell cycle arrest and apoptosis after DNA damage independently of p53.

2002 ◽  
Vol 277 (23) ◽  
pp. 21110 ◽  
Author(s):  
Damu Tang ◽  
Dongcheng Wu ◽  
Atsushi Hirao ◽  
Jill M. Lahti ◽  
Lieqi Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Erk Activation ◽  
Cycle Arrest

scholarly journals P28-10 Cisplatin induces DNA damage associated with cell cycle arrest and apoptosis in PC9 cells

2021 ◽  
Vol 32 ◽  
pp. S346
Author(s):  
Md Mohiuddin ◽  
Hideharu Kimura ◽  
Takashi Sone ◽  
Hiroki Matsuoka ◽  
Keigo Saeki ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Cycle Arrest

scholarly journals Aqueous Extracts of the Edible Gracilaria tenuistipitata are Protective Against H2O2-Induced DNA Damage, Growth Inhibition, and Cell Cycle Arrest

Molecules ◽  
2012 ◽  
Vol 17 (6) ◽  
pp. 7241-7254 ◽  
Author(s):  
Jing-Iong Yang ◽  
Chi-Chen Yeh ◽  
Jin-Ching Lee ◽  
Szu-Cheng Yi ◽  
Hurng-Wern Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Aqueous Extracts ◽  
Damage Growth ◽  
Gracilaria Tenuistipitata ◽  
Cycle Arrest

Mollugin induced oxidative DNA damage via up-regulating ROS that caused cell cycle arrest in hepatoma cells

2022 ◽  
pp. 109805
Author(s):  
Xin-ge Ke ◽  
Yi-yi Xiong ◽  
Bing Yu ◽  
Chong Yuan ◽  
Peng-yu Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Oxidative Dna Damage ◽  
Hepatoma Cells ◽  
Cycle Arrest

NCPMF-60 induces G2/M cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells

2011 ◽  
Vol 22 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Qin-Sheng Dai ◽  
Wei Liu ◽  
Xiao-Bing Wang ◽  
Na Lu ◽  
Dan-Dan Gong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
M Cell ◽  
Cycle Arrest

Octadecyloxyethyl Adefovir Exhibits Potent in vitro and in vivo Cytotoxic Activity and Has Synergistic Effects with Ara-C in Acute Myeloid Leukemia

Chemotherapy ◽  
2018 ◽  
Vol 63 (4) ◽  
pp. 225-237 ◽  
Author(s):  
Haytham Khoury ◽  
Ruijuan He ◽  
Aaron Schimmer ◽  
James R. Beadle ◽  
Karl Y. Hostetler ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Acute Myeloid Leukemia ◽  
Cell Cycle Arrest ◽  
Clinical Benefit ◽  
Myeloid Leukemia ◽  
Mouse Bone Marrow ◽  
Medical Needs ◽  
Cycle Arrest ◽  
Acute Myeloid

Acute myeloid leukemia (AML) continues to be a deadly disease, with only 50–70% of patients achieving complete remission and less than 30% of adults having sustained long-term remissions. In order to address these unmet medical needs, we carried out a high-throughput screen of an in-house library of on- and off-patent drugs with the OCI/AML-2 cell line. Through this screen, we discovered adefovir dipi­voxil (adefovir-DP) as being active against human AML. In addition to adefovir-DP, there are second-generation formulations of adefovir, including octadecyloxyethyl adefovir (ODE-adefovir) and hexadecyloxypropyl adefovir (HDP-adefovir), which were designed to overcome the pharmacokinetic problems of the parent compound adefovir. Given the known clinical benefit of nucleoside analogs for the treatment of AML, we undertook studies to evaluate the potential benefit of adefovir-based molecules. In AML cell lines and patient samples, adefovir-DP and ODE-adefovir were highly potent, whereas HDP-adefovir was significantly less active. Interestingly, ODE-adefovir was remarkably less toxic than adefovir-DP towards normal hematopoietic cells. In addition, ODE-adefovir at a dose of 15 mg/kg/day showed potent activity against human AML in a NOD/SCID mouse model, with a reduction of human leukemia in mouse bone marrow of > 40% in all mice tested within 20 days of treatment. Based on its chemical structure, we hypothesized that the cytotoxicity of ODE-adefovir toward AML was through cell cycle arrest and DNA damage. Indeed, ODE-adefovir treatment induced cell cycle arrest in the S phase and increased levels of pH2Ax, indicating the induction of DNA damage. Furthermore, there was an increase in phospho-p53, transactivation of proapoptotic genes and activation of the intrinsic apoptotic pathway. Subsequent investigation unveiled strong synergism between ODE-adefovir and ara-C, making their coadministration of potential clinical benefit. Expression of MRP4, a nucleoside transporter, appeared to influence the response of AML cells to ODE-adefovir, as its inhibition potentiated ODE-adefovir killing. Taken together, our findings indicate that clinical development of ODE-adefovir or related compounds for the treatment of AML is warranted.

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