1. Academic Validation
  2. Shikonin Induces Autophagy and Apoptosis in Esophageal Cancer EC9706 Cells by Regulating the AMPK/mTOR/ULK Axis

Shikonin Induces Autophagy and Apoptosis in Esophageal Cancer EC9706 Cells by Regulating the AMPK/mTOR/ULK Axis

  • Anal Cell Pathol (Amst). 2024 Oct 29:2024:7752299. doi: 10.1155/2024/7752299.
Junli Zhang 1 2 Jiayi Guo 2 Biao Gu 1 Fen Wang 1 Yi Li 1 Ling Shang 2 Wendi Jiang 2 Junrao Ma 2 Wenjuan Wu 3
Affiliations

Affiliations

  • 1 Bengbu Third People's Hospital Affiliated to Bengbu Medical University, Bengbu 233030, Anhui, China.
  • 2 Bengbu Medical University Key Laboratory of Cancer Research and Clinical Laboratory Diagnosis, Bengbu Medical University, Bengbu 233030, Anhui, China.
  • 3 Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical University, Bengbu 233030, Anhui, China.
Abstract

Shikonin is a plant medicine extracted from Lithospermum, which dominate influential antioxidant and antitumor effect. Here, we report that shikonin was capable of inducing human esophageal Cancer EC9706 cell Apoptosis and Autophagy, in a time- and dose-dependent manner. Shikonin exposure repressed cell viability and migration and invasion capabilities and caused EC9706 cell Autophagy and Apoptosis by activating the AMPK/mTOR/ULK axis. Autophagy inhibition secured EC9706 cells against shikonin-induced Autophagy and Apoptosis and reversed the upregulation of AMPK and ULK phosphorylation and downregulation of mTOR phosphorylation provoked by shikonin. In summary, shikonin instigates EC9706 cell Apoptosis and Autophagy using the target AMPK/mTOR/ULK signal pathway axis, which provides a potential new target to treat human esophageal Cancer.

Keywords

apoptosis; autophagy; esophageal cancer; shikonin; the AMPK/mTOR/ULK axis.

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