J Cancer 2022; 13(7):2050-2060. doi:10.7150/jca.65875 This issue

Research Paper

Cucurbitacin I inhibits the proliferation of pancreatic cancer through the JAK2/STAT3 signalling pathway in vivo and in vitro

Dongchao Xu1,2,3, Hongzhang Shen1,2,3, Mengyao Tian1, Wangyang Chen1, Xiaofeng Zhang1,2,3✉

1. Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou310000, China.
2. Hangzhou Institute of Digestive Diseases, Hangzhou310000, China.
3. Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou310000, China.

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Citation:
Xu D, Shen H, Tian M, Chen W, Zhang X. Cucurbitacin I inhibits the proliferation of pancreatic cancer through the JAK2/STAT3 signalling pathway in vivo and in vitro. J Cancer 2022; 13(7):2050-2060. doi:10.7150/jca.65875. Available from https://www.jcancer.org/v13p2050.htm

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Abstract

Graphic abstract

Pancreatic cancer is one of the most aggressive solid malignancies, as it has a 5-year survival rate of less than 10%. The growth and invasion of pancreatic cancer cells into normal tissues and organs make resection and treatment difficult. Finding an effective chemotherapy drug for this disease is crucial. In this study, we selected the tetracyclic triterpenoid compound cucurbitacin I, which may be used as a potential therapeutic drug for treating pancreatic cancer. First, we found that cucurbitacin I inhibited pancreatic cancer proliferation in a dose-time dependent manner. Further studies have shown that cucurbitacin I blocks the cell cycle of pancreatic cancer in the G2/M phase and induces cell apoptosis. In addition, under the action of the compound, the invasion ability of cells was greatly reduced and markedly impaired the growth of pancreatic tumour xenografts in nude mice. Furthermore, the decrease in pancreatic cancer cell proliferation caused by cucurbitacin I appeared to involve JAK2/STAT3 signalling pathway inhibition, and the use of JAK2/STAT3 activators effectively restored the inhibition. In conclusion, our research may provide a basis for the further development of pancreatic cancer treatment drugs.

Keywords: Cucurbitacin I, pancreatic cancer, JAK2/STAT3 signalling pathway, proliferation