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In-depth mechanistic study of a newly synthesized non-platinum-naproxen complex as an anti-cancer agent

Date

20 Dec 2015

Session

Poster presentation 2

Presenters

Jolly Deb

Citation

Annals of Oncology (2015) 26 (suppl_9): 37-39. 10.1093/annonc/mdv521

Authors

J. Deb1, T.R. Lakshman2, T.K. Paine2, S.S. Jana3

Author affiliations

  • 1 Biological Chemistry, indian association for the cultivation of science, 700032 - Kolkata/IN
  • 2 Inorganic Chemistry, indian association for the cultivation of science, Kolkata/IN
  • 3 Biological Chemistry, indian association for the cultivation of science, Kolkata/IN
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Resources

Abstract 779

Aim/Background

The role of Epithelial–mesenchymal transition (EMT) in cancer progression is now well documented, and the search for new anti-cancer drugs that could hinder EMT pathway is of utmost importance to develop a more effective treatment regime. In this context, we have evaluated the candidature of a synthesized prodrug (80-N) on human breast cancer cell line (MDA-MB-231).

Methods

Highly invasive MDA-MB-231 cells were treated with non-platinum- naproxen complex in vitro, and the underlying mechanism of action was explored by employing studies related to induction of apoptosis, activation of caspases, cellular migration, regulation of EMT markers, anchorage independent growth, and disruption of tubular structure on matrigel.

Results

It was apparent from the apoptosis assay that 80-N induced growth inhibitory activity on MDA-MB-231 cells was due to an early induction of apoptosis followed by subsequent induction of caspases 3 and 9. The prodrug could also halt cellular migration, and on further investigation it was evident that cellular architecture was disrupted and vimentin was down regulated following treatment. Moreover, 80-N was capable of hindering colony formation on soft-agar, and also disrupted the tubular network on extra-cellular-matrix (ECM).

Conclusions

In this study we report that the non-platinum- naproxen complex (80-N) is an anti-EMT drug with properties to induce significant amount of apoptosis in breast cancer cell line. Since the drug can also delay cancer cell (MDA-MB-231) migration, and disrupt tubular network formation on ECM, we can safely conclude that it would in turn delay cellular invasion and metastatic spread of the cancer cells. Thus, we propose that the therapeutic potential of 80-N is worthy of further investigation in an in vivo animal model.

Clinical trial identification

Disclosure

All authors have declared no conflicts of interest.

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