University of Tabriz

Acute myocardial infarction (AMI) has been recognized as a leading cause of death, posing a significant threat to human health for decades. The assessment of cardiac troponin I (cTnI), an important biomarker for AMI, has demonstrated superior sensitivity and specificity in diagnosing myocardial damage. This research aims to establish a particularly sensitive and inexpensive electrochemical aptasensor for cTnI detection. The biosensing system was constructed utilizing a custom-made cell featuring a gold (Au) substrate, which exploits an innovative signal amplification approach involving ciprofloxacin (Cip) loaded into UIO-66 metal-organic framework (MOF). The measurement of the electrochemical oxidation current of released Cip molecules that is proportional to cTnI concentrations was accomplished with the differential pulse voltammetry (DPV) technique. The developed aptasensor exhibited an extremely low detection limit of 2.05 aM and a wide dynamic range, spanning from 3.14 aM to 314.0 pM. Additionally, the successful determination of cTnI in the presence of other blood proteins, such as myoglobin, human serum albumin (HSA), hemoglobin, and immunoglobulin G (IgG), demonstrates the high selectivity of the developed aptasensor. Moreover, in vitro studies of serum samples from patients with cardiac injury and healthy individuals demonstrated the aptasensor's capability in detecting cTnI at ultra-low concentrations, which could facilitate the early detection of cardiac injury.

Cancer cells are considered the most adaptable for their metabolic status, which supports growth, survival, rapid proliferation, invasiveness, and metastasis in a nutrient-deficient microenvironment. Since the discovery of altered glucose metabolism (aerobic glycolysis), which is generally known as a part of metabolic reprogramming and an innate trait of cancer cells, in 1930 via Dr. Otto Warburg, numerous studies have endeavored to recognize various aspects of cancer cell metabolism and find new methods for efficiently eradicating described cells by targeting their energy metabolism. In this way, the outcomes have mainly been promising. Accordingly, outlining the related results will indeed assist us in making a definitive path for developing targeted therapy strategies based on cancer cell-altered metabolism. The present study reviews the key features of cancer cell metabolism and treatment strategies based on them. It emphasizes the importance of targeting cancer cell dysregulated metabolic pathways that influence the cell energy supply and manage cancer cell growth and survival. This trial also introduces a multimodal therapeutic strategy hypothesis, a potential next-generation combination therapy approach, and suggests interdisciplinary research to recognize the complexities of cancer metabolism and exploit them for designing more efficacious cancer therapeutic strategies.

Melanoma, a form of skin cancer, develops as a result of melanocytes growing malignantly. The global incidence of melanoma is on the rise, posing significant public health challenges. Consequently, it holds the highest fatality rate among skin cancers and accounts for the majority of deaths. Accurately classifying the stages of this cancer is a crucial yet arduous task, particularly during patient diagnosis. Cancer stem cells, which are a type of tumor-initiating cell, have been extensively researched for their rapid proliferation, migration, and contribution to cancer recurrence. These cells, characterized by specific markers such as CD133, possess a significantly heightened ability to initiate cancer, making them crucial in developing therapeutic strategies. The current study intended to determine the CD133 siRNA impact on angiogenesis, apoptosis, migration, proliferation, and stemness characteristics in melanoma cancer in the SK-MEL3 cell line.

For this purpose, the wound healing test was used to evaluate the cells' migratory potential, and the results indicated a decrease in the migration rate. Colony formation assays were also done to measure the stemness properties, which showed decreased stemness features in SK-MEL3 cells. Furthermore, the qRT-PCR and western blot assays demonstrated that the CD133 silencing reduced its expression and gene expression in migration and stemness. Finally, co-culturing HUVEC cells with SK-MEL3 cells, which suppressed CD133 expression, decreased the expression of angiogenic genes.

This study highlights the therapeutic potential of CD133-siRNA in tumor treatment, warranting further investigation in future animal and clinical trials.