Apoptosis induced anticancer potential of aspirin on A549 Carcinoma Cell
Keywords:
Aspirin (ASA), A549 lung cancer cells, 5-Fluorouracil (5-FU)Abstract
Recent research has discovered that using aspirin for a long time lowers the long-term risk of certain cancers, particularly colon cancer. However, the mechanism of anti-cancerous activity of aspirin against lung cancer is less studied. A molecular docking strategy was employed to identify the possible targets of aspirin while5-Fluorouracil (5-FU) was used as a positive control against lung cancer cell line A459. The In-silico analysis suggested that Caspase-3, Bax, andBcl-2could be potential targets for aspirin. The estimation of binding energies for these proteins resulted in -5.2, -5.8, and -5.7 Kcal/mol, respectively, which were better than 5FU (-4.8, -4.6, and -4.4, respectively).Trypan blues dye exclusion test exhibited a reduction in cell viability with the increase in Aspirin concentration. The IC50 values of Aspirin were calculated as 2.79 mM by MTT assay. The treatment of A459 cells with aspirin enhanced the levels of apoptotic genes at mRNA as well as at protein levels. The effect on the A549 lung cancer cell line, this study contributes to a better understanding of how Aspirin and 5-FU work in lung cancer.
Downloads
References
S. C. Gupta, B. Sung, S. Prasad, L. J. Webb, and B. B. Aggarwal, Cancer drug discovery by repurposing: teaching new tricks to old dogs, Trends in pharmacological sciences, (2013), 34(9), 508–517.
R. L. Siegel, K. D. Miller, and A. Jemal, Cancer statistics, CA: a cancer journal for clinicians, (2018), 68(1), 7–30.
N. Zakaria, N. A. Satar, N. H. Abu Halim, S. H. Ngalim, N. M. Yusoff, J. Lin, and B. H. Yahaya, Targeting Lung Cancer Stem Cells: Research and Clinical Impacts, Frontiers in oncology, (2017), 7, 80.
National Center for Biotechnology Information, PubChem Compound Summary for CID 2244, Aspirin. Retrieved July 4, 2021 from https://pubchem.ncbi.nlm.nih.gov/compound/Aspirin, (2021),
A. M. Algra, and P. M. Rothwell, Effects of regular aspirin on long-term cancer incidence and metastasis: a systematic comparison of evidence from observational studies versus randomised trials, The Lancet. Oncology, (2012), 13(5), 518–527.
C. Bosetti, V. Rosato, S. Gallus, J. Cuzick, and C. La Vecchia, Aspirin and cancer risk: a quantitative review to 2011, Annals of oncology : official journal of the European Society for Medical Oncology, (2012), 23(6), 1403–1415.
M. Gomes, A. L. Teixeira, A. Coelho, A. Araújo, and R. Medeiros, The role of inflammation in lung cancer. Advances in experimental medicine and biology, (2014), 816, 1–23.
Q. Liu, Q. Tan, , Y. Zheng, K. Chen, C. Qian, N. Li, Q. Wang, and X. Cao, Blockade of Fas signaling in breast cancer cells suppresses tumor growth and metastasis via disruption of Fas signaling-initiated cancer-related inflammation, The Journal of biological chemistry, (2014), 289(16), 11522–11535.
E. Elinav, R. Nowarski, C. A. Thaiss, B. Hu, C. Jin, and R. A. Flavell, Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms, Nature reviews. Cancer, (2013), 13(11), 759–771.
K. T. Wilson, S. Fu, K. S. Ramanujam, and S. J Meltzer, Increased expression of inducible nitric oxide synthase and cyclooxygenase-2 in Barrett's esophagus and associated adenocarcinomas, Cancer research, (1998), 58(14), 2929–2934.
K. C. Zimmermann, M. Sarbia, A. A. Weber, F. Borchard, H. E. Gabbert, and K. Schrör, Cyclooxygenase-2 expression in human esophageal carcinoma, Cancer research, (1999), 59(1), 198–204.
M. A. Kern, M. M. Schöneweiss, D. Sahi, M. Bahlo, A. M. Haugg, H. U. Kasper, H. P. Dienes, H. Käferstein, K. reuhahn, and P . Schirmacher, Cyclooxygenase-2 inhibitors suppress the growth of human hepatocellular carcinoma implants in nude mice, Carcinogenesis, (2004), 25(7), 1193–1199.
T. L. Larkins, M. Nowell, S. Singh, and G. L. Sanford, Inhibition of cyclooxygenase-2 decreases breast cancer cell motility, invasion and matrix metalloproteinase expression”, BMC cancer, (2006), 6, 181.
S. K. Banu, J. Lee, V. O. Speights, A. Starzinski-Powitz, and J. A. Arosh, Cyclooxygenase-2 regulates survival, migration, and invasion of human endometriotic cells through multiple mechanisms”, Endocrinology, (2008), 149(3), 1180–1189.
R. Ali-Fehmi, R. T. Morris, S. Bandyopadhyay, M. Che, V. Schimp, J. M. Malone, and A. R. Munkarah, Expression of cyclooxygenase-2 in advanced stage ovarian serous carcinoma: correlation with tumor cell proliferation, apoptosis, angiogenesis, and survival, American journal of obstetrics and gynecology, (2005), 192(3), 819–825.
M. T. Rizzo, Cyclooxygenase-2 in oncogenesis, Clinica chimica acta; international journal of clinical chemistry, (2011), 412(9-10), 671–687.
J. Y. Yhee, S. Son, H. Lee, and K. Kim, Nanoparticle-Based Combination Therapy for Cancer Treatment, Current pharmaceutical design, (2015), 21(22), 3158–3166.
Y. Ge, Y. Ma, & L. Li, The application of prodrug-based nano-drug delivery strategy in cancer combination therapy , Colloids and surfaces. B, Biointerfaces, (2016), 146, 482–489.
T. Wang, R. Narayanaswamy, H. Ren, and V. P. Torchilin, Combination therapy targeting both cancer stem-like cells and bulk tumor cells for improved efficacy of breast cancer treatment, Cancer biology & therapy, (2016), 17(6), 698–707.
J. Lin, L. Wu, X. Bai, Y. Xie, A. Wang, H. Zhang, X. Yang, X. Wan, X. Lu, X. Sang, and H. Zhao, Combination treatment including targeted therapy for advanced hepatocellular carcinoma”, Oncotarget, (2016), 7(43), 71036–71051.
F. V. Din, A. Valanciute, V. P. Houde, D. Zibrova, K. A. Green, K. Sakamoto, D. R. Alessi, and M. G. Dunlop, Aspirin inhibits mTOR signaling, activates AMP-activated protein kinase, and induces autophagy in colorectal cancer cells, Gastroenterology, (2012), 142(7), 1504–15.
P. Dikshit, M. Chatterjee, A. Goswami, A. Mishra, NR. Jana, Aspirin induces apoptosis through the inhibition of proteasome function, J. Biol. Chem, (2006), 281, 29228–29235.
M. Lu, A. Strohecker, F. Chen, T. Kwan, J. Bosman, VC. Jordan, VL. Cryns, Aspirin sensitizes cancer cells to TRAIL-induced apoptosis by reducing survivin levels, Clin Cancer Res, (2008), 14(10):3168-76.
T. Mosmann, Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays, Journal of immunological methods, (1983), 65(1-2), 55–63.
M. B. Hansen, S. E. Nielsen, and K. Berg, Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill, Journal of immunological methods, (1989), 119(2), 203–210.
AT. Chan, S. Ogino, CS. Fuchs, Aspirin use and survival after diagnosis of colorectal cancer, JAMA, (2009), 302: 649–58.
BH. Choi, G. Chakraborty, K. Baek, HS. Yoon, Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells, Exp Mol Med, (2013), 45(10):e47.
G. Sitia, M. Iannacone, LG. Guidotti, Anti-platelet therapy inthe prevention of hepatitis B virus-associated hepatocellularcarcinoma, J Hepatol, (2013), 59: 1135–8.
HC. Thoms, MG. Dunlop, LA. Stark. p38‐mediated inactivation of cyclin D1/cyclin‐dependent kinase 4 stimulates nucleolar translocation of RelA and apoptosis in colorectal cancer cells. Cancer Res, (2007), 67, 1660–1669.
J.S. Shiff, M.I. Koutsos, L. Qiao, B. Rigas, Nonsteroidal antiinflammatory drugs inhibit the proliferation of colon adenocarcinoma cells: effects on cell cycle and apoptosis, Exp. Cell Res, (1996), 179–188.
S.C. Williams, W. Smalley, R.N. Dubois, Aspirin use and potential mechanisms for colorectal cancer prevention, J. Clin. Invest, (1997), 1325–1329.
Published
How to Cite
Issue
Section
Copyright (c) 2022 International journal of health sciences
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Articles published in the International Journal of Health Sciences (IJHS) are available under Creative Commons Attribution Non-Commercial No Derivatives Licence (CC BY-NC-ND 4.0). Authors retain copyright in their work and grant IJHS right of first publication under CC BY-NC-ND 4.0. Users have the right to read, download, copy, distribute, print, search, or link to the full texts of articles in this journal, and to use them for any other lawful purpose.
Articles published in IJHS can be copied, communicated and shared in their published form for non-commercial purposes provided full attribution is given to the author and the journal. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgment of its initial publication in this journal.
This copyright notice applies to articles published in IJHS volumes 4 onwards. Please read about the copyright notices for previous volumes under Journal History.