Background: In cancer cells, apoptosis is an important mechanism that influences the outcome of chemotherapy and the development of chemoresistance. To find the genes involved in chemoresistance and the development of gastric cancer, we used the suppression subtractive hybridization method to identify the genes that are overexpressed in gastric cancer tissues compared to normal gastric tissues. Results: In the suppression subtractive hybridization library we constructed, the most highly overexpressed genes were humanin isoforms. Humanin is a recently identified endogenous peptide that has anti-apoptotic activity and has been selected for further study due to its potential role in the chemoresistance of gastric cancer. Upregulation of humanin isoforms was also observed in clinical samples by using quantitative real-time PCR. Among the studied isoforms, humanin isoform 3, with an expression level of 4.166 ± 1.44 fold, was the most overexpressed isoform in GC. Conclusions: The overexpression of humanin in gastric cancer suggests a role for chemoresistance and provides new insight into the biology of gastric cancer. We propose that humanin isoforms are novel targets for combating chemoresistance in gastric cancer.

Salmonella is a foodborne pathogen of animal and public health significance. Considering the disadvantages of antibiotics or chemical preservatives traditionally used to eliminate this pathogen, attention has shifted, in recent years, toward biocontrol agents such as bacteriophages, used either separately or in combination to prevent food contamination. However, extensive use of phage-based biocontrol agents in the food industry requires further studies to ensure their safety and efficacy. In the present study, we investigated the effectiveness and safety of phage cocktail, a phage cocktail comprising three pre-characterized Salmonella phages (vB_SenS_TUMS_E4, vB_SenS_TUMS_E15 and vB_SenS_TUMS_E19). First, we performed an MTT [3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide] assay on a human foreskin fibroblast cell line, in which the resulting high cell viability revealed the safety of the phage cocktail. Next, we performed a time-kill assay in which a 4 Log decline in bacterial levels was detected. Additionally, we utilized a colorimetric method to evaluate the anti-biofilm activity of phage cocktail, in which it proved more efficacious compared to the MIC and MBEC levels of the antibiotic control. Then, we assessed the ability of phage cocktail to eradicate Salmonella in different food samples, where it considerably reduced the bacterial count regardless of the temperature (4°C and 25°C). Lastly, we used broiler chickens as an animal model to measure the growth-promoting activity of phage cocktail. Salmonella-infected chickens orally treated with modified phage cocktail demonstrated no mortality and a significant increase in weight gain compared to the untreated group (p ≤ 0.0002). The study presents a novel research evaluating the effectiveness and safety of a phage cocktail as a biocontrol agent against Salmonella in various contexts, including biofilms, food products, and broiler chickens. This multifaceted approach underscores the promising role of phage therapy as a sustainable biocontrol strategy in food safety and public health contexts.

To find genes involved in tumorigenesis and the development of esophageal cancer, the suppression subtractive hybridization (SSH) method was used to identify genes that are overexpressed in esophageal cancer tissues compared to normal esophageal tissues. In our SSH library, the forkhead box O3 (FOXO3), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and myeloid differentiation primary response 88 (MYD88) genes were the most highly upregulated genes, and they were selected for further studies because of their potential role in the induction of autophagy. Upregulation of these genes was also observed in clinical samples using qRT-PCR. In addition, coexpression analysis of the autophagy-related genes Beclin1, ATG12, Gabarapl, PIK3C3, and LC3 demonstrated a significant correlation between the differentially overexpressed genes and autophagy. Autophagy is an important mechanism in tumorigenesis and the development of chemoresistance in cancer cells. The upregulation of FOXO3, GAPDH, and MYD88 variants in esophageal cancer suggests a role for autophagy and provides new insight into the biology of esophageal cancer. We propose that FOXO3, GAPDH, and MYD88 are novel targets for combating autophagy in esophageal cancer.

Background: Using molecular adjuvants offers an attractive strategy to augment DNA vaccine-mediated immune responses. Several studies have revealed that an efficient HCV vaccine model should be able to induce both humoral and cell mediated immune responses targeting the conserved regions of the virus to circumvent the immune escape mutants. The beta chemokine Macrophage Inflammatory Protein 3-beta (MIP-3beta) is a key modulator of dendritic cells (DCs) and T-cells interaction, functions during immune response induction and is secreted specifically by cells in the lymphoid tissues. Objectives: In the present study, we questioned whether co-administration of MIP-3beta gene could enhance the immune responses to HCV core in DNA vaccination. Materials and Methods: Expression and biological activity of MIP-3beta expressing plasmid were evaluated by ELISA and transwell migration assays, respectively. HCV core DNA vaccine ± plasmid expressing MIP-3beta were electroporated subcutaneously to the front foot pads of BALB/c mice on days 0 and 14, and HCV core protein booster was applied to all core-DNA-vaccine received mice on the day 28. Both cell mediated immunity (proliferation, IFN-γ and IL-4 cytokine release, IFN-γ ELISpot and cytotoxic Granzyme B release assays) and humoral immune responses (total IgG and IgG2a/IgG1 subtyping) were evaluated ten days after final immunization. Results: Mice covaccinated with MIP-3beta elicited an enhanced Th1 biased systemic immune response as evidenced by higher IFN-γ/IL-4 and anti-core IgG2a/IgG1 ratio, lymphoproliferation, strong cytolytic GrzB release and enhanced population of IFN-γ producing immunocytes. Likewise, the humoral immune response assumed as the total anti-core IgG level was augmented by MIP-3beta co-delivery. Conclusions: These results exhibited the immuno potentiator effects of MIP-3beta plasmid when coadministrated with the HCV core DNA vaccine. Complimentary studies integrating MIP-3beta as a genetic adjuvant in HCV-core-DNA vaccination models are warranted. Keywords: Chemokine CCL19; Hepatitis C; Hepatitis C Antigens; Adjuvants