The Association between Dietary Protein Intake and the Risk of Pancreatic Cancer: Evidence from 14 Publications.

Many studies have been published to assess the association about dietary protein intake on the risk of pancreatic cancer, but with inconsistent result. This meta-analysis aimed to evaluate whether protein intake could affect the risk of pancreatic cancer. A systematic literature search was performed in PubMed, EMBASE and Web of Science up to October 1, 2019. Pooled relative risks (RR) and 95% confidence intervals (CI) were calculated using a random-effect model. A total of 14 studies (12 case-control studies and two cohort studies) were included. Overall, total protein intake had no significant association on the risk of pancreatic cancer (RR = 1.02, 95%CI= 0.85-1.22, I2=45.7%). Subgroup analyses showed such relationships were almost not influenced by study design and geographic location. Interestingly, when we performed the subgroup analysis by protein type, the opposite association was found in animal protein intake (RR = 1.37, 95%CI= 0.93-2.01) and vegetable protein intake (RR = 0.78, 95%CI= 0.54-1.14), although these two groups were not statistically significant. In conclusion, this meta-analysis indicated that dietary total protein intake may be not associated with the risk of pancreatic cancer. However, protein type may be affecting the result which was found from our research. Therefore, studies with detailed information, especially protein type, are warranted to further confirm these findings.

CGA-N12, a peptide derived from chromogranin A, promotes apoptosis of Candida tropicalis by attenuating mitochondrial functions.

CGA-N12 (the amino acid sequence from the 65th to the 76th residue of the N-terminus of chromagranin A) is an antifungal peptide derived from human chromogranin A (CGA). In our previous investigation, CGA-N12 was found to have specific anti-candidal activity, though the mechanism of action remained unclear. Here, we investigated the effects of CGA-N12 on mitochondria. We found that CGA-N12 induced an over-generation of intracellular reactive oxygen species and dissipation in mitochondrial membrane potential, in which the former plays key roles in the initiation of apoptosis and the latter is a sign of the cell apoptosis. Accordingly, we assessed the apoptosis features of Candida tropicalis cells after treatment with CGA-N12 and found the following: leakage of cytochrome c and uptake of calcium ions into mitochondria and the cytosol; metacaspase activation; and apoptotic phenotypes, such as chromatin condensation and DNA degradation. In conclusion, CGA-N12 is capable of inducing apoptosis in C. tropicalis cells through mitochondrial dysfunction and metacaspase activation. Antifungal peptide CGA-N12 from human CGA exhibits a novel apoptotic mechanism as an antifungal agent.