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Acetyl-11-Keto-β-Boswellic Acid Exerts the Anti-Cancer Effects via Cell Cycle Arrest, Apoptosis Induction and Autophagy Suppression in Non-Small Cell Lung Cancer Cells

Authors Lv M, Shao S, Zhang Q, Zhuang X, Qiao T

Received 28 October 2019

Accepted for publication 9 January 2020

Published 23 January 2020 Volume 2020:13 Pages 733—744


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Minghe Lv, Shali Shao, Qi Zhang, Xibing Zhuang, Tiankui Qiao

Center for Tumor Diagnosis and Therapy, Jinshan Hospital, Fudan University, Shanghai 201508, People’s Republic of China

Correspondence: Tiankui Qiao
Center for Tumor Diagnosis and Therapy, Jinshan Hospital, Fudan University, Jinshan District, Shanghai 201508, People’s Republic of China
Email [email protected]

Objective: Acetyl-11-keto-β-boswellic acid (AKBA) is a triterpenoid, which is the main component of boswellic acid from Boswellia Serrata, a medicinal plant that has shown immense potential in anti-cancer therapy. This study aims to explore the roles and molecular mechanisms of AKBA on cell behavior in non-small cell lung cancer (NSCLC) cells.
Materials and Methods: The effects of AKBA on the cell viability in A549, H460, H1299, and BEAS-2B cells were determined by the CCK-8 assay. The colony formation assay was used to identify the effects of AKBA on cell proliferation. Potential roles of AKBA in regulating the cell cycle, apoptosis, and autophagy in A549 were evaluated by flow cytometry, Western blotting, reverse transcription-polymerase chain reaction (PCR) and immunofluorescence (IF).
Results: AKBA reduced cell viability in A549, H460, H1299, and BEAS-2B. In A549 cells, AKBA suppressed the clone formation, arrested the cell cycle at the G0/G1 phase, induced cellular apoptosis. We found that AKBA suppressed the formation of autolysosome, and decreased the expression levels of Beclin-1, LC3A/B-I, and LC3A/B-II proteins. Furthermore, AKBA also inhibited the expression levels of PI3K/Akt signaling pathway proteins.
Conclusion: AKBA exerts the anti-cancer effects via cell cycle arrest, apoptosis induction, and autophagy suppression in NSCLC cells. This body of evidence supports the potential of AKBA as a promising drug in the treatment of NSCLC.

Keywords: Acetyl-11-keto-β-boswellic acid, cell cycle, apoptosis, autophagy, non-small cell lung cancer

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