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Activation of CaMKKβ-AMPK-mTOR Pathway Is Required for Autophagy Induction by β,β-dimethylacrylshikonin Against Lung Adenocarcinoma Cells

Activation of CaMKKβ-AMPK-mTOR Pathway Is Required for Autophagy Induction by β,β-dimethylacrylshikonin Against Lung Adenocarcinoma Cells

Haibing Wang, Gaochenxi Zhang

Biochem Biophys Res Commun. 2019 Sep 24;517(3):477-483.

PMID: 31376944

Abstract:

β,β-Dimethylacrylshikonin (DMAS), an active ingredient of Lithospermum erythrorhizon and Arnebia euchroma, possess anti-neoplasm properties. Recently, DMAS was reported to stimulate autophagy in lung adenocarcinoma cells. However, the mechanisms by which DMAS modulates autophagy. have not yet been clearly elucidated. In this study, we found that DMAS significantly elevated intracellular free calcium accumulation. This activated the CaMKKβ-AMPK-mTOR pathway, subsequently inhibited mTOR and its substrate p70s6k and 4E-BP1, eventually leading to autophagy. In addition, we demonstrated that inhibition of autophagy by BAPTA-AM or STO-609 or compound C potently enhanced DMAS-induced lung adenocarcinoma cells apoptosis and growth inhibition. Overall, our results suggested that cytoprotective autophagy was triggered by DMAS via CaMKKβ-AMPK-mTOR signaling cascade in human lung adenocarcinoma cells, meaning that combining use of DMAS and autophagy inhibitors as a novel therapeutic option for lung adenocarcinoma will be very promising.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4246396	4EBP1 Active human			Price

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