Abstract
To investigate the possible mechanism of Qingyihuaji formula (QYHJ) for reversing gemcitabine (GEM) resistant human pancreatic cancer. Cell proliferation, apoptosis, migration and invasion were detected in CFPAC-1 cells. Xenograft mice established with CFPAC-1 through subcutaneous on 33 immunodeficient nude mice and randomly divided into four groups: vehicle, GEM (35 mg/kg), QYHJ (40 g/kg), and GEM + QYHJ (35 mg/kg + 40 g/kg) groups for 28-day treatment. Tumor growth and the mRNA expression of lncRNA AB209630, miR373, EphB2, and NANOG evaluated in dissected tumor tissue by real-time PCR, the CD133+ cancer stem cells were isolated by flow cytometer, and the changes of the tumor sphere forming were measured. QYHJ, especially the combination of GEM and QYHJ, was significantly inhibited the cell proliferation and migration of CFPAC-1 in vitro in the indicated times. The combination of GEM and QYHJ also remarkably promoted the cell apoptosis of CFPAC-1. QYHJ treatment effectively blocked the tumor growth in nude mice. QYHJ, especially GEM + QYHJ treatment, was significantly increased the mRNA expression of lncRNA AB209630, significantly decreased the mRNA levels of miR373, EphB2 and NANOG, and markedly reduced the tumor sphere formation and the numbers of CD133+ stem cells. In addition, GEM alone treatment had no significant effect in the above biomarker changes. QYHJ could effectivly enhance the antihuman pancreatic tumor activity of GEM, which may be through inhibiting pancreatic cancer stem cell differentiation by lncRNA AB209630/miR-373/EphB2-NANOG signaling pathway.
Highlights
Pancreatic cancer is one of the most common malignant tumors in the digestive system [1]
In the combination of GEM and Qingyihuaji formula (QYHJ) treatment group, cell proliferation inhibitory effects were dramatically increased in the longer of the treatment times (24, 48, and 72h) than GEM or QYHJ alone treatment, which implied that QYHJ could enhance the activity of GEM in the pancreatic cancer cell
We detected the cell proliferation inhibition of QYHJ in normal hTERT-HPNE cells, the result indicated that there has a slightly cell proliferation inhibition, but no significant difference compared with the control group (Supplementary Figure S1)
Summary
Pancreatic cancer is one of the most common malignant tumors in the digestive system [1]. 85% of pancreatic cancer patients die within 1 year after diagnosis, and the 5-year survival rate is less than 50% [2]. Pancreatic cancer mainly originates from pancreatic ductal cell malignancies, which are more common in people aged 50–60, and the incidence of male is higher than that of female [4]. The incidence of pancreatic cancer has shown a steady upward trend at home and abroad – an increase of about 15% every 10 years. About 80% of pancreatic cancer patients have metastasis when symptoms appear [3,4]. Some data show that the incidence of pancreatic cancer in the world is about 185,000 per year, while the incidence of pancreatic cancer in China has increased fourfold in 20 years, reaching 51/100,000 [5]
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