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Combinatorial Chemistry & High Throughput Screening

Editor-in-Chief

ISSN (Print): 1386-2073
ISSN (Online): 1875-5402

Research Article

Neobavaisoflavone Demonstrates Valid Anti-tumor Effects in Non-Small- Cell Lung Cancer by Inhibiting STAT3

Author(s): Xueding Cai, Feng Zhou, Xiaona Xie, Dandan Zheng, Yulei Yao, Chengguang Zhao*, Xiaoying Huang* and Ke Hu*

Volume 25, Issue 1, 2022

Published on: 04 December, 2020

Page: [29 - 37] Pages: 9

DOI: 10.2174/1386207323666201204135941

Price: $65

Abstract

Aim and Objective: Lung cancer is the most commonly occurring cancer, which contributes to the majority of death caused by cancer, where non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer. To treat NSCLC, STAT3 has been identified as a target with therapeutic potential. The neobavaisoflavone (NBIF) is one of the flavonoids of traditional Chinese medicine Psoralea corylifolial.

Materials and Methods: Human NSCLC cell lines, PC-9, H460, and A549, were applied to determine NBIF’s anti-proliferative effects through cell viability and colony formation detection. The effect of NBIF on cell apoptosis was determined through flow cytometry-based assay. Western blotting was used in this study to confirm the levels of P-STAT3, Bcl-2, and Bax, which are apoptotic proteins.

Results: It was observed that NBIF could decrease the cell viability and its migration and induce apoptosis in human NSCLC cell lines dose-dependently. Levels of P-STAT3, as well as the downstream signals of the STAT3 pathway, were downregulated, suggesting that the tumorsuppression effects of NBIF might be related to the inhibition of STAT3 signaling. Furthermore, NBIF could contribute to the upregulation of BAX and downregulation of BCL2.

Conclusion: NBIF might perform the anti-NSCLC efficacy as a result of the inhibition of the STAT3 pathway. Besides, our work suggests that NBIF could provide therapeutic alternatives for NSCLC.

Keywords: Neobavaisoflavone, NSCLC, STAT3, apoptosis, antitumor, pathology.

Graphical Abstract

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