RETRACTED: Isoquercitrin inhibits the progression of pancreatic cancer in vivo and in vitro by regulating opioid receptors and the mitogen-activated protein kinase signalling pathway (Retracted article. See vol. 49, 2023)

被引:60
|
作者
Chen, Quan [1 ]
Li, Ping [1 ,2 ]
Li, Ping [1 ,2 ]
Xu, Yong [1 ]
Li, Yang [3 ]
Tang, Bo [3 ]
机构
[1] Liaoning Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Jinzhou 121001, Liaoning, Peoples R China
[2] Liaoning Med Univ, Affiliated Hosp 1, Dept Oncol, Jinzhou 121001, Liaoning, Peoples R China
[3] Guilin Med Univ, Dept Hepatobiliary Surg & Med Oncol, Affiliated Hosp, Guilin 541001, Guangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
isoquercitrin; opioid receptor; pancreatic cancer; signalling pathway; ENZYMATICALLY MODIFIED ISOQUERCITRIN; BIDENS-BIPINNATA L; DIFFERENTIAL REGULATION; CELL-PROLIFERATION; GENE-EXPRESSION; C-JUN; APOPTOSIS; HEPATOCARCINOMA; ANTICANCER; RESISTANCE;
D O I
10.3892/or.2014.3626
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic cancer is a common malignant tumour that affects individuals worldwide. In recent years, the incidence and mortality rates of pancreatic cancer have continuously increased. Currently, the primary clinical treatment methods for pancreatic cancer include surgical resection, chemotherapy and radiotherapy. However, these treatment methods rarely produce satisfactory therapeutic outcomes. Extensive research has also proven that the effective components of several traditional Chinese medicines, particularly flavonoids extracted from plants, have significant antitumour effects. Isoquercitrin, which is one of the flavonoids found in Bidens pilosa extracts, has a significant antitumour effect. However, the antitumour effect of isoquercitrin and its mechanism of action remain unclear. The objective of the present study was to investigate the effect of isoquercitrin on the progression of pancreatic cancer and to further understand the biological characteristics of the participation of isoquercitrin in the progression of pancreatic cancer. In vitro, we found that a therapeutic dose of isoquercitrin significantly inhibited proliferation, promoted apoptosis and induced cell cycle arrest within the 01 phase in pancreatic cancer cells. Isoquercitrin activated caspase-3, -8 and -9 and reduced the mitochondrial membrane potential. In addition, isoquercitrin inhibited the expression level of the delta opioid receptor; however, isoquercitrin had no effect on the kappa and mu opioid receptors. Furthermore, isoquercitrin inhibited extracellular signal-regulated kinase (ERK) phosphorylation and promoted c-Jun N-terminal kinase (JNK) phosphorylation. In vivo, we found that a therapeutic dose of isoquercitrin significantly inhibited xenograft growth in nude mice. In summary, the present study demonstrated that isoquercitrin inhibits human pancreatic cancer progression in vivo and in vitro and that its molecular mechanism may be closely related to opioid receptors and to the activation of the mitogen-activated protein kinase (MAPK) signalling pathway.
引用
收藏
页码:840 / 848
页数:9
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