Arsenite promotes centrosome abnormalities under a p53 compromised status induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)

Toxicology and Applied Pharmacology
Wei-Ting LiaoLouis W Chang

Abstract

Epidemiological evidence indicated that residents, especially cigarette smokers, in arseniasis areas had significantly higher lung cancer risk than those living in non-arseniasis areas. Thus an interaction between arsenite and cigarette smoking in lung carcinogenesis was suspected. In the present study, we investigated the interactions of a tobacco-specific carcinogen 4- (methylnitrosamino)-1-(3-pyridyl)-1-butanone (nicotine-derived nitrosamine ketone, NNK) and arsenite on lung cell transformation. BEAS-2B, an immortalized human lung epithelial cell line, was selected to test the centrosomal abnormalities and colony formation by NNK and arsenite. We found that NNK, alone, could enhance BEAS-2B cell growth at 1-5 microM. Under NNK exposure, arsenite was able to increase centrosomal abnormality as compared with NNK or arsenite treatment alone. NNK treatment could also reduce arsenite-induced G2/M cell cycle arrest and apoptosis, these cellular effects were found to be correlated with p53 dysfunction. Increased anchorage-independent growth (colony formation) of BEAS-2B cells cotreated with NNK and arsenite was also observed in soft agar. Our present investigation demonstrated that NNK could provide a p53 compromised status. Arseni...Continue Reading

References

Jun 1, 1997·Mutation Research·M M MooreC L Doerr
Dec 23, 1998·Mutagenesis·G P PfeiferM Tang
Oct 31, 2000·Epidemiology·C FerreccioA H Smith
Jan 5, 2002·The Journal of Dermatology·H S YuY L Guo
May 15, 2003·Molecular Biotechnology·Barbara G Campling, Wafik S El-Deiry
Dec 11, 2003·Proceedings of the National Academy of Sciences of the United States of America·Frederique ZindyCharles J Sherr
May 1, 2004·American Journal of Public Health·Yu Chen, Habibul Ahsan
May 4, 2004·Trends in Pharmacological Sciences·Edmund Maser
Jul 28, 2004·Toxicology and Applied Pharmacology·Toby G RossmanFredric J Burns
Aug 24, 2004·Oncogene·Paolo Boffetta
Nov 19, 2004·Nature·Scott W LoweGerard Evan
Nov 27, 2004·Toxicological Sciences : an Official Journal of the Society of Toxicology·Hanspeter Witschi
Dec 23, 2004·JAMA : the Journal of the American Medical Association·Chi-Ling ChenUNKNOWN Blackfoot Disease Study Group
Jan 18, 2005·Seminars in Cancer Biology·Sergei N Rodin, Andrei S Rodin
May 14, 2005·Cell Biology International·Stefan Duensing
Jun 22, 2005·Toxicology and Applied Pharmacology·Chien-Jen ChenMeei-Maan Wu
Dec 17, 2005·Epidemiology·Chikako KiyoharaYoichi Nakanishi
Oct 20, 2007·Toxicology and Applied Pharmacology·Wei-Ting LiaoLouis W Chang
Feb 12, 2008·Trends in Pharmacological Sciences·Richard D EgletonPiyali Dasgupta

❮ Previous
Next ❯

Citations

Nov 2, 2011·International Journal of Biological Sciences·Jason Yongsheng Chan
Sep 15, 2011·The Kaohsiung Journal of Medical Sciences·Wei-Ting LiaoHsin-Su Yu
Oct 11, 2011·Toxicology and Applied Pharmacology·Chao-Yuan HuangYu-Mei Hsueh
Dec 2, 2010·Biochemical Society Transactions·Amie L Holmes, John Pierce Wise
Dec 2, 2010·Biochemical Society Transactions·Sandra S Wise, John Pierce Wise

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Cancer Genomics (Keystone)

Cancer genomics approaches employ high-throughput technologies to identify the complete catalog of somatic alterations that characterize the genome, transcriptome and epigenome of cohorts of tumor samples. Discover the latest research using such technologies in this feed.

Cell Checkpoints & Regulators

Cell cycle checkpoints are a series of complex checkpoint mechanisms that detect DNA abnormalities and ensure that DNA replication and repair are complete before cell division. They are primarily regulated by cyclins, cyclin-dependent kinases, and the anaphase-promoting complex/cyclosome. Here is the latest research.

Related Papers

Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology
Kathryn TerryImmaculata De Vivo
© 2022 Meta ULC. All rights reserved