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Original Research Article | OPEN ACCESS

Quinolinol-platinum (II) complex suppresses survival and invasion of laryngeal cancer cells via targeting YES-associated protein expression

Baotong Xie1, Tao Li2

1Department of Otolaryngology; 2Department of Ophthalmology, Lvliang People's Hospital, Lvliang Hospital Affiliated of Shanxi Medical University, Lvliang 033000, Shanxi Province, China.

For correspondence:-  Tao Li   Email: KinsleyWeisseuu@yahoo.com

Accepted: 22 July 2020        Published: 31 August 2020

Citation: Xie B, Li T. Quinolinol-platinum (II) complex suppresses survival and invasion of laryngeal cancer cells via targeting YES-associated protein expression. Trop J Pharm Res 2020; 19(8):1625-1630 doi: 10.4314/tjpr.v19i8.9

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the anti-proliferative potential of quinolinol-platinum (II) complex {QN-Pt (II)} in laryngeal cancer cells.
Methods: The inhibitory potential of QN-Pt (II) on the proliferation of laryngeal cancer cells was determined using 2H-tetrazolium, 2-(4,5-dimethyl-2-thiazolyl)-3,5-diphenyl bromide (MTT) and colony formation assays. Inhibition of cell migration was determined using wound-healing assay, while changes in LC3-II and p62 expressions were assessed by western blotting.
Results: QN-Pt (II) inhibited the viability of TU212 and M4e laryngeal cancer cells in the concentration range of 2 to 10 µM (p < 0.05). Moreover, it suppressed the colony formation potential and migration of TU212 and M4e cells. The QN-Pt (II) treatment increased the proportion of TU212 and M4e cells in G1/G0 phase of the cell cycle, but decreased the cell proportion in S and G2/M phase (p < 0.05). Treatment with 10 µM QN-Pt (II) increased the expression of LC3?II, but downregulated P62 expression in TU212 and M4e cells. The expression of Yes-associated protein was inhibited in TU212 and M4e cells on treatment with QN-Pt (II). However, transfection of YAP-cDNA into TU212 and M4e cells reversed the inhibitory effect of QN-Pt (II) on cell proliferation (p < 0.05). Moreover, YAP-cDNA transfection suppressed LC3II expression, inhibited YAP phosphorylation and promoted P62 expression in QN-Pt (II)-treated TU212 and M4e cells (p < 0.05).
Conclusion: QN-Pt (II) suppresses laryngeal cancer cell viability via arrest of cell cycle and activation of apoptosis. Moreover, QN-Pt (II) targets Yes-associated protein in laryngeal cancer cells. Thus, QN-Pt (II) is a potential therapeutic agent for laryngeal cancer.

Keywords: Laryngeal cancer, YAP-protein, Apoptosis, Phosphorylation, Therapeutic agent

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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