TSPAN1 silencing protects against cerulein-induced pancreatic acinar cell injury via targeting AGR2.

Acute pancreatitis (AP) is an inflammatory gastrointestinal disorder affecting the pancreas. Previous study reported that tetraspanin 1 (TSPAN1) expression was significantly upregulated in the pancreas of AP patients. However, the underlying molecular mechanism of TSPAN1 in the pathogenesis of AP remains unclear. Thus, the aim of the present study was to investigate the potential role of TSPAN1 in development of AP. RT-qPCR was carried out to quantify the relative mRNA levels of TSPAN1 and anterior gradient-2 (AGR2). The CCK-8 assay was used to detect the cell viability. The TUNEL assay was performed to visualize the apoptotic cells. Western blot was performed to determine the expressions of proteins related to endoplasmic reticulum (ER) stress and apoptosis. ELISA kits were adopted to detect the concentration of inflammatory cytokines including TNF-α and IL-6. Finally, immunoprecipitation (IP) was used to verify the interaction between TSPAN1 and AGR2. TSPAN1 was upregulated in serum of AP patients and AP cell models. TSPAN1 silencing promoted the cell proliferation and inhibited inflammatory response in cerulein-induced AR42J cells. Moreover, TSPAN1 induced endoplasmic reticulum stress by binding AGR2. Interestingly, the overexpression of AGR2 abolished the effects of TSPAN1 silencing on cell proliferation and inflammatory response in cerulein-induced AR42J cells. In summary, TSPAN1 silencing protects against cerulein-induced pancreatic acinar cell injury through inhibiting ER stress-mediated by AGR2. Hence, TSPAN1 may serve as a promising therapeutic target for AP treatment.

Randomly controlled study of chemotherapy versus chemoimmunotherapy in postoperative lung cancer patients.

A randomly controlled study of chemotherapy versus chemoimmunotherapy was performed in patients with operable lung cancer from November 1977 to June 1981. The immunotherapy consisted of an intrapleural instillation of Nocardia rubra cell wall skeleton (N-CWS) followed by serial intradermal N-CWS. A total of 119 patients were entered into this trial. There were 64 evaluable patients in the control group and 52 evaluable patients in the N-CWS group. N-CWS treatment was effective in terms of prolongation of duration of remission for all operable patients. Although significant improvement in the survival rate was not observed in patients at Stages I and II (p less than 0.10), it was observed in the curative operation group (p less than 0.05). The mode of recurrence was classified as local recurrence and distant metastasis in the curative operation group. The rates of distant metastasis were 34.0 and 18.9%, respectively, in the control and the N-CWS groups. The rate of local recurrence was 14.9% in the control group; however, no local recurrence was observed in the N-CWS group. These results indicate the clinical effectiveness of the N-CWS treatment, especially in curatively resectable lung cancer. No serious side effect was observed during this trial.