Investigation of GNB1 derivative circular RNAs hsa_circ_0009361 and hsa_circ_0009362 expressions in colorectal cancer patients: potential new diagnostic factors.

Aim: We aim to investigate the relationship between hsa_circ_0009361 plus hsa_circ_0009362 expression levels and the clinicopathological features of colorectal cancer (CRC) patients. Background: Circular RNAs (circRNAs) are implicated in the progression and development of CRC. CircRNAs have been recognized as diagnostic and prognostic biomarkers, opening up a new window to comprehend the molecular basis of CRC. Given the significance of circRNAs and the G protein subunit b1 (GNB1) gene in malignancies, the goal of the current investigation was to determine the expression levels of GNB1 derivative circular RNAs circGNB1 (hsa_circ_0009361 and hsa_circ_0009362) in CRC and adjacent control tissues. Methods: The expression levels of the GNB1 derivative circular RNAs (hsa_circ_0009361 and hsa_circ_0009362) were evaluated using the quantitative real-time PCR (qRT-PCR) method in 45 CRC tissues and adjacent control tissues. Furthermore, we analyzed the diagnostic power of the mentioned circRNAs by plotting the receiver operating characteristic (ROC) curve. The association between the expression levels of hsa_circ_0009361 and hsa_circ_0009362 was evaluated using correlation analysis. Results: Our results revealed that the expression levels of hsa_circ_0009361 and hsa_circ_0009362 were significantly down-regulated in CRC tissues compared to the adjacent control group. Analysis of patients' clinicopathological features indicated that expressions of hsa_circ_0009361 and hsa_circ_0009362 were differently related to lymph vascular invasion (P<0.001). ROC curve results showed that these circRNAs are good candidate diagnostic biomarkers in CRCs. Pearson's correlation test revealed a positive correlation between hsa_circ_0009361 and hsa_circ_0009362 expression levels (P<0.0001). Conclusion: These results demonstrated that hsa_circ_0009361 and hsa_circ_0009362 expression levels may be used as possible diagnostic biomarkers for CRC.

Gene expression profile of Campylobacter jejuni in response to macrolide antibiotics.

Campylobacter jejuni is a foodborne pathogen that causes gastroenteritis in humans and has developed resistance to various antibiotics. The primary objective of this research was to examine the network of antibiotic resistance in C. jejuni. The study involved the wild and antibiotic-resistant strains placed in the presence and absence of antibiotics to review their gene expression profiles in response to ciprofloxacin via microarray. Differentially expressed genes (DEGs) analysis and Protein-Protein Interaction (PPI) Network studies were performed for these genes. The results showed that the resistance network of C. jejuni is modular, with different genes involved in bacterial motility, capsule synthesis, efflux, and amino acid and sugar synthesis. Antibiotic treatment resulted in the down-regulation of cluster genes related to translation, flagellum formation, and chemotaxis. In contrast, cluster genes involved in homeostasis, capsule formation, and cation efflux were up-regulated. The study also found that macrolide antibiotics inhibit the progression of C. jejuni infection by inactivating topoisomerase enzymes and increasing the activity of epimerase enzymes, trying to compensate for the effect of DNA twisting. Then, the bacterium limits the movement to conserve energy. Identifying the antibiotic resistance network in C. jejuni can aid in developing drugs to combat these bacteria. Genes involved in cell division, capsule formation, and substance transport may be potential targets for inhibitory drugs. Future research must be directed toward comprehending the underlying mechanisms contributing to the modularity of antibiotic resistance and developing strategies to disrupt and mitigate the growing threat of antibiotic resistance effectively.

The role of interferon-gamma and its receptors in gastrointestinal cancers.

Gastrointestinal malignancies are the most prevalent type of cancer around the world. Even though numerous studies have evaluated gastrointestinal malignancies, the actual underlying mechanism is still unknown. These tumors have a poor prognosis and are frequently discovered at an advanced stage. Globally, there is an increase in the incidence and mortality of gastrointestinal malignancies, including those of the stomach, esophagus, colon, liver, and pancreas. Growth factors and cytokines are signaling molecules that are part of the tumor microenvironment and play a significant role in the development and spread of malignancies. IFN-γ induce its effects by activation of intracellular molecular networks. The main pathway involved in IFN-γ signaling is the JAK/STAT pathway, which regulates the transcription of hundreds of genes and mediates various biological responses. IFN-γ receptor is composed of two IFN-γR1 chains and two IFN-γR2 chains. Binding to IFN-γ, causes the intracellular domains of IFN-γR2 to oligomerize and transphosphorylate with IFN-γR1 which activates downstream signaling components: JAK1 and JAK2. These activated JAKs phosphorylate the receptor, creating binding sites for STAT1. STAT1 is then phosphorylated by JAK, resulting in the formation of STAT1 homodimers (gamma activated factors or GAFs) that translocate to the nucleus and regulate gene expression. The balance between positive and negative regulation of this pathway is crucial for immune responses and tumorigenesis. In this paper, we evaluate the dynamic roles of IFN- γ and its receptors in gastrointestinal cancers and present evidence that inhibiting IFN- γ signaling may be an effective treatment strategy.