Introduction: Antimicrobial resistance is alarmingly high because it happens in humans, environment, and animal sectors from a "One Health" viewpoint. Due to the fact, that Escherichia coli (E. coli) is broadly disseminated in all sectors, the food web and the environment may have a role in carrying colistin resistance genes from animals to humans. The rise of plasmid-mediated mobile colistin resistance (MCR) genes threatens colistin efficacy, which is the last line to remedy Gram-negative infections multidrug resistance (MDR). Objectives: The current study aimed to investigate development of colistin resistance (MCR 1-5) genes between E. coli isolated from patients with urinary tract infections (UTI) in Jordan. Methods: E. coli (n=132) isolated were collected from urine specimens. E. coli isolated from human UTI patients were examined for genes resistance to colistin MCR (1-5). All isolates were investigated against 20 antimicrobials utilizing the standard disk diffusion method. For analysis of colistin resistance, the broth microdilution technique was employed. In addition, the MCR (1-5) genes were detected by multiplex PCR assay. Results: Out of 132 isolates, one isolate was colistin-resistant, having a minimum inhibitory concentration of 8 μg/mL and possessing the MCR -1 gene. A total of 132 E. coli isolates showed high resistance against penicillin, amoxicillin, cephalexin, nalidixic acid, tetracycline, and cefepime in the percentages of 100%, 79.55%, 75.76%, 62.88%, 58.33%, and 53.79%, respectively. However, resistance was lowest towards fosfomycin (6.06%), florfenicol (10.61%), and chloramphenicol (15.91%). Significant differences were observed between E. coli isolated from pediatrics and those isolated from adults. Conclusion: This is the first report on the presence of the plasmid-coded MCR-1 gene recovered from E. coli from a patient with UTIs in Jordan. That is threatening as colistin is the last line used for infections induced by MDR gram-negative bacteria. There is a crucial need for control and harsh utilization of antibiotics to control and prevent the emergence and prevalence of colistin resistance genes.