Tumorigenic effect of interleukin-6 on mice with pancreatic carcinoma via regulating the Caspase-3 / Bax / Bcl-2 signaling pathway / 解剖学报

ABSTRACT

Objective To explore the tumorigenic effect of interleukin(IL)-6 on mice with pancreatic carcinoma and the Caspase-3 / Bax / Bcl-2 signaling pathway related mechanism. Methods Forty mice were used to establish tumor-bearing animal model of pancreatic cancer with mouse pancreatic cancer cell line MPC-83. The tumor-bearing mice were divided into blank control group (A), intraperitoneal injection PBS 10 ml / kg; IL-6 group (B), intraperitoneal injection recombinant mouse IL-6 200 μg / kg; IL-6 receptor blocker group (C), intraperitoneal injection tocilizumab 100 mg / kg; and IL-6 + IL-6 receptor blocker group (D), intraperitoneal injection tocilizumab 100 mg / kg, 30 minutes later, intraperitoneal injection recombinant mouse IL-6 200 μg / kg, 10 mice in each group. The mice in each group were administrated corresponding drug once every 3 days for 28 days. The tumor volume was to observe and record at day 0, 7, 14, 21 and 28 after the experiment began. The mice were sacrificed by cervical vertebra dislocation after the last measurement of tumor volume. ELISA method was used to test the contents of survivin and cytochrome C (Cyt-C) in transplanted tumor tissue of mice. Reverse transcription polymerase chain reaction (RT-PCR) and Western blotting method were used to detect the expression levels of Caspase-3, Bax and Bcl-2 mRNA and protein in transplanted tumor tissue of mice. Results Compared with the A group, the transplanted tumor tissue of mice in group B grew rapidly on day 7, 14, 21 and 28, the content of survivin was increased, the content of Cyt-C was decreased, the expression levels of Caspase-3 and Bax mRNA and protein was down-regulated, and the expression levels of Bcl-2 mRNA and protein was up-regulated (P 0. 05). Conclusion The role of IL-6 in promoting the growth and proliferation of pancreatic cancer may be related to the regulation of Caspase-3/ Bax/ Bcl-2 cell apoptosis signaling pathway.