Objective: To research the inhibitory effect on SGC-7901 cells of α -pinene, and the related mechanism of α -pinene. Methods: Used the MTT method to detect inhibition rate and western blotting to detect the influence on expression of ATM, Phos-S1981ATM, H2AX, γ H2AX, CHK2 and p-CHK2, p53 and phos-p53 cell cycle related protein in SGC-7901 cells. Results: The research found α -pinene could inhibit the proliferation of SGC-7901 cells observably in vitro , and the inhibition rate assumes the dependence on concentration; and western blotting results showed that, α -pinene could activate phospho-ATM, increase the amount of γ H2AX ( p < 0.05, p < 0.05); increase the expression of p-CHK2, p53 and phos-p53 ( p < 0.05, p < 0.05, p < 0.05); But there is no significant effect on expression of CHK2 ( p > 0.05). Conclusions: α -pinene could inhibit the proliferation of SGC-7901 cells, and by inducing ATM (Ataxia Telangiectasia-Mutated) kinase signal pathway in DNA damage response, activating cell cycle checkpoint, making the cell cycle arrest then exerts its anti-tumor effects.
Bhattacharjee, B. and Chatterjee, J. (2013) Identification of Proapoptopic, Anti-Inflammatory, Anti-Proliferative, Anti-Invasive and Anti-Angiogenic Targets of Essential Oils in Cardamom by Dual Reverse Virtual Screening and Binding Pose Analysis. Asian Pacific Journal of Cancer Prevention, 14, 3735-3742. http://www.apocpcontrol.org/page/apjcp_issues_view.php?sid=Entrez:PubMed&id=pmid :23886174&key=2013.14.6.3735 http://dx.doi.org/10.7314/APJCP.2013.14.6.3735
Boohaker, R.J. and Xu, B. (2014) The Versatile Functions of ATM Kinase. Biomedical Journal, 37, 3-9. http://dx.doi.org/10.4103/2319-4170.125655
Kusuhara, M., Urakami, K., Masuda, Y., Zangiacomi, V., Ishii, H., Tai, S., Maruyama, K. and Yamaguchi, K. (2012) Fragrant Environment with α-Pinene Decreases Tumor Growth in Mice. Biomedical Research, 33, 57-61. https://www.jstage.jst.go.jp/article/biomedres/33/1/33_1_57/_article
Singh, H.P., Batish, D.R., Kaur, S., Arora, K. and Kohli, R.K. (2006) Alpha-Pinene Inhibits Growth and Induces Oxidative Stress in Roots. Annals of Botany, 98, 1261-1269. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803591/ http://dx.doi.org/10.1093/aob/mcl213
Chen, W.-Q., Xu, B., Wei, F.X., Li, M., Liu, T., Jin, X.B. and Zhang, L.R. (2014) Inhibitory Effects of α-Pinene on Hepatoma Carcinoma Cell Proliferation. Asian Pacific Journal of Cancer Prevention, 15, 3293-3297. http://www.apocpcontrol.org/page/apjcp_issues_view.php?sid=Entrez:PubMed&id=pmid :24815485&key=2014.15.7.3293
Wajs, A., Urbańska, J., Zaleskiewicz, E. and Bonikowski, R. (2010) Composition of Essential Oil from Seeds and Cones of Abies alba. Natural Product Communications, 5, 1291-1294.
Wang, B. (2014) Analyzing Cell Cycle Checkpoints in Response to Ionizing Radiation in Mammalian Cells. Methods in Molecular Biology, 1170, 313-320. http://www.ncbi.nlm.nih.gov/pubmed/24906320 http://dx.doi.org/10.1007/978-1-4939-0888-2_15
Ling, H., Lu, L.F., He, J., et al. (2014) Diallyl Disulfide Selectively Causes Checkpoint Kinase-1 Mediated G2/M Arrest in Human MGC803 Gastric Cancercell Line. Oncology Reports, 32, 2274-2282. http://www.spandidos-publications.com/or/32/5/2274
Zeng, Q.Y., Zeng, L.J., Huang, Y., et al. (2014) 8-60hIPP5(m)-Induced G2/M Cell Cycle Arrest Involves Activation of ATM/p53/p21(cip1/waf1) Pathways and Delayed Cyclin B1 Nuclear Translocation. Asian Pacific Journal of Cancer Prevention, 15, 4101-4107. http://www.ncbi.nlm.nih.gov/pubmed/24935604 http://dx.doi.org/10.7314/APJCP.2014.15.9.4101
Zhao, P., Chen, L., Li, L.H., Wei, Z.F., Tong, B., Jia, Y.G., Kong, L.Y., Xia, Y.F. and Dai, Y. (2014) SC-III3, a Novel Scopoletin Derivative, Induces Cytotoxicity in Hepatocellular Cancer Cells through Oxidative DNA Damage and Ataxia Telangiectasia-Mutated Nuclear Protein Kinase Activation. BMC Cancer, 19, 987. http://www.ncbi.nlm.nih.gov/pubmed/25527123
Wei, F., Yan, J. and Tang, D. (2011) Extracellular Signal-Regulated Kinases Modulate DNA Damage Response—A Contributing Factor to Using MEK Inhibitors in Cancer Therapy. Current Medicinal Chemistry, 18, 5476-5482. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3330700/ http://dx.doi.org/10.2174/092986711798194388
Sowd, G.A., Mody, D., Eggold, J., Cortez, D., Friedman, K.L. and Fanning, E. (2014) SV40 Tilizes ATM Kinase Activity to Prevent Non-Homologous End Joining of Broken Viral DNA Replication Products. PLoS Pathogens, 10, e1004536. http://www.ncbi.nlm.nih.gov/pubmed/25474690 http://dx.doi.org/10.1371/journal.ppat.1004536
Yao, G., Qi, M., Ji, X., Fan, S., Xu, L., Hayashi, T., Tashiro, S., Onodera, S. and Ikejima, T. (2014) ATM-p53 Pathway Causes G2/M Arrest, but Represses Apoptosis in Pseudolaric Acid B-Treated HeLa Cells. Archives of Biochemistry and Biophysics, 5, 51-60. http://dx.doi.org/10.1016/j.abb.2014.05.029
Wei, F.X., Xie, Y.Y., Tao, L.J. and Tang D. (2010) Both ERK1 and ERK2 Kinases Promote G2/M Arrest in Etoposide-Treated MCF7 Cells by Facilitating ATM Activation. Cellular Signalling, 22, 1783-1789. http://dx.doi.org/10.1016/j.cellsig.2010.07.007
Akihisa, T., Eiichiro, M., Nakagawa, Y., Okamoto, N., Uemura, H., Kondo, N., Noda, T., Toki, A., Ejima, Y., Chen, D.J., Ohnishi, K. and Ohnishi, T. (2010) ATM Is the Predominant Kinase Involved in the Phosphorylation of Histone H2AX after Heating. Journal of Radiation Research, 51, 417-422. http://jrr.oxfordjournals.org/content/51/4/417.long
Mamouni, K., Cristini, A., Guirouilh-Barbat, J., Monferran, S., Lemarié, A., Faye, J.C., Lopez, B.S., Favre, G. and Sordet, O. (2014) RhoB Promotes γH2AX Dephosphorylation and DNA Double-Strand Break Repair. Molecular and Cellular Biology, 34, 3144-3155. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135599/ http://dx.doi.org/10.1128/MCB.01525-13
Ma, Y.C., Su, N., Shi, X.J., Zhao, W., Ke, Y., Zi, X., Zhao, N.M., Qin, Y.H., Zhao, H.W. and Liu, H.M. (2015) Jaridonin-Induced G2/M Phase Arrest in Human Esophageal Cancer Cells Is Caused by Reactive Oxygen Species-Dependent Cdc2-tyr15 Phosphorylationvia ATM-Chk1/2-Cdc25C Pathway. Toxicology and Applied Pharmacology, 282, 227-236. http://www.ncbi.nlm.nih.gov/pubmed/25450480 http://dx.doi.org/10.1016/j.taap.2014.11.003
Lossaint, G., Besnard, E., Fisher, D., Piette, J. and Dulic, V. (2011) Chk1 Is Dispensable for G2 Arrest in Response to Sustained DNA Damage When the ATM/p53/p21 Pathway Is Functional. Oncogene, 30, 4261-4274. http://www.ncbi.nlm.nih.gov/pubmed/21532626 http://dx.doi.org/10.1038/onc.2011.135
Abdel-Fatah, T.M., Arora, A., Alsubhi, N., Agarwal, D., Moseley, P.M., Perry, C., Doherty, R., Chan, S.Y., Green, A.R., Rakha, E., Ball, G., Ellis, I.O. and Madhusudan, S. (2014) Clinicopathological Significance of ATM-Chk2 Expression in Sporadic Breast Cancers: A Comprehensive Analysis in Large Cohorts. Neoplasia, 16, 982-991. http://www.ncbi.nlm.nih.gov/pubmed/25425972 http://dx.doi.org/10.1016/j.neo.2014.09.009