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Abstract

Calycosin Inhibits Pancreatic Cancer Cell Proliferation, Migration and Invasion by Repressing Circ_0000285

Author(s): Ruibing Ma, Xiaoping Yu and Kun Cheng*
Characteristic Specialty One Group Department, Xinjiang Municipal Corps Hospital Chinese People’s Armed Police Force (CAPF), 1Department of Pancreatic Surgery, Digestive and Vascular Surgical Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830000, China

Correspondence Address:
Kun Cheng, Department of Pancreatic Surgery, Digestive and Vascular Surgical Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830000, China, E-mail: 18199324449@163.com


Recent studies have shown that calycosin possess multiple pharmacological properties, containing anti-cancer activity. Hence, this project explored the effect and possible mechanism of calycosin in pancreatic cancer. After being cultured, SW1990 cells were exposed to different concentrations of calycosin. 3-(4,5-dimethylthiazol 2-yl)-2,5 diphenyl tetrazolium bromide, plate colony formation, and transwell experiments assessed cell proliferation, colony formation, migration, and invasion. Circ_0000285 expression was assessed using quantitative reverse transcription-polymerase chain reaction experiment. E-cadherin and N-cadherin protein levels were examined using Western blot. After calycosin treatment, SW1990 cell proliferation, migration, invasion, circ_0000285 expression, N-cadherin were repressed, and E-cadherin was increased in dose-dependent way. Circ_0000285 deficiency might hinder cell proliferation, migration, and invasion. Furthermore, the upregulation of circ_0000285 might partly antagonize calycosin-mediated SW1990 cell proliferation, migration, and invasion inhibition. Calycosin treatment might block pancreatic cancer cell development through down-regulating circ_0000285.

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