RESUMO
Background and aim: Adenosine A1 receptor (AA1R) has been shown to have an inhibitory effect on cell growth in several cancers; however, its function in esophageal cancer is still unclear. In this study, we examined the effect of AA1R on cell growth and apoptosis in esophageal cancer cells. Materials and methods: In this study, YM-1 and KYSE-30 esophageal cancer cell lines were cultured. AA1R gene expression was determined by quantitative Real-time Polymerase Chain Reaction (qRT-PCR). As well, the AA1R antagonist (DPCPX) effect on cell viability was evaluated by the MTT assay. Moreover, apoptosis was assessed by annexin-V and propidium iodide staining, and the caspase-3/7 activity assay kit. Result: qRT-PCR results indicated that the AA1R was expressed in YM-1 and KYSE-30 cells. In addition, DPCPX significantly decreased cell proliferation in both cell lines. Furthermore, the A1AR antagonist induced apoptosis in KYSE-30 and YM-1 cells. After treatment of both cell lines with DPCPX, the caspase 3/7 activity was increased. Conclusion: Our finding indicates the AA1R antagonist induces apoptosis through caspase 3/7 activation and can be considered a potential target in esophageal cancer therapy.
RESUMO
Background and Objectives: One of the major causes of urinary tract infections is Klebsiella pneumoniae. Currently, few studies investigated the mechanisms of resistance to colistin in Iran. The current study aimed to determine the prevalence of plasmid and chromosome-mediated resistance to colistin in K. pneumoniae isolates. Materials and Methods: 177 urine samples were collected from patients with urinary tract infections hospitalized in the intensive care unit (ICU) of hospitals in the city of Qazvin. K. pneumoniae isolates were identified by standard biochemical methods, resistance to colistin among K. pneumoniae isolates were tested by disk diffusion and microbroth dilution methods. The chromosomal mutation and presence of the mcr genes in colistin-resistant K. pneumoniae were evaluated by PCR. Results: Out of 177 samples, 65 K. pneumoniae were obtained from patients in the ICU. Six colistin-resistant isolates were isolated with MIC values ≥4 µg/mL, none of them was positive for mcr1-5. In 4 isolates, missense mutation in mgrB gene resulted in amino acid substitutions and in one isolate of mgrB gene was found intact mgrB gene. Conclusion: The results suggest that mgrB mutation was the main mutation among colistin-resistant isolates and plasmid-borne colistin resistance was not expanded among strains.
RESUMO
BACKGROUND: Today, the pancreatic cancer prognosis is poor and genetic technology is developing to treat various types of cancers. Scientists are actively looking for a new technique to design a therapeutic strategy to treat pancreatic cancer. Several oncolytic viruses are known to be valuable tools for pancreatic cancer treatment. Recent Studies demonstrate their effectiveness and safety in various administration routes such as direct intratumoral, intracutaneous, intravascular, and other routes. METHOD: In this study, all studies conducted in the past 20 years have been reviewed. Reputable scientific databases including Irandoc, Scopus, Google Scholar and PubMed, are searched for the keywords of Pancreatic cancer, oncolytic, viruses and treatment and the latest information about them is obtained. RESULTS: Engineering the oncolytic viruses' genome and insertion of intended transgenes including cytokines or shRNAs, has caused promising promotions in pancreatic cancer treatment. Some oncolytic viruses inhibit tumors directly and some through activation of immune responses. CONCLUSION: This approach showed some signs of success in efficiency like immune system activation in the tumor environment, effective virus targeting in the tumor cells by systemic administration, and enhanced patient survival in comparison with the control group. But of course, until now, using these oncolytic viruses alone has not been effective in elimination of tumors.
