Apoptosis induced anticancer potential of aspirin on A549 Carcinoma Cell

https://doi.org/10.53730/ijhs.v6nS1.7248

Authors

  • Abu Junaid Department of Biotechnology, Faculty of Engineering and Technology Rama University, G.T. Road, Kanpur-209217, India
  • Ajay Kumar Department of Biotechnology, Faculty of Engineering and Technology Rama University, G.T. Road, Kanpur-209217, India

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

Download data is not yet available.

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

12-05-2022

How to Cite

Junaid, A., & Kumar, A. (2022). Apoptosis induced anticancer potential of aspirin on A549 Carcinoma Cell. International Journal of Health Sciences, 6(S1), 9611–9626. https://doi.org/10.53730/ijhs.v6nS1.7248

Issue

Section

Peer Review Articles

Most read articles by the same author(s)