Metabolic reprogramming is a well-known feature of cancer that allows malignant cells to alter metabolic reactions and nutrient uptake, thereby promoting tumor growth and spread. It has been discovered that noncoding RNAs (ncRNAs), including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), have a role in a variety of biological functions, control physiologic and developmental processes, and even influence disease. They have been recognized in numerous cancer types as tumor suppressors and oncogenic agents. The role of ncRNAs in the metabolic reprogramming of cancer cells has recently been noticed. We examine this subject, with an emphasis on the metabolism of glucose, lipids, and amino acids, and highlight the therapeutic use of targeting ncRNAs in cancer treatment.

Ulcerative colitis (UC) and Crohn's disease (CD) are two major forms of inflammatory bowel disease (IBD), which is an inflammatory disease. Studies have shown that adipose tissue and inflammation play important roles in the pathogenesis of IBD. C1q/TNF‐related protein‐3 (CTRP3) is a newly discovered adipokine playing a substantial role during inflammatory process, and for the first time in the present study, serum levels of this adipokine were measured in the UC and CD patients. This case–control study included 70 control, 50 UC, and 50 CD patients who were diagnosed by standard criteria. Serum levels of adiponectin, IL‐6, TNF‐α, TGF‐β, and CTRP3 were evaluated using ELISA kits. Serum levels of IL‐6, TNF‐α, and TGF‐β elevated in the UC and CD patients compared with the controls while adiponectin and CTRP3 diminished in the patient's groups compared with the control. Furthermore, decrease in CTRP3 serum levels was associated with the risk of UC and CD diseases. Moreover, CTRP3 indicated negative correlation with BMI, FBS, insulin, homeostasis model assessment of insulin resistance, IL‐6, TNF‐α, and TGF‐β and also a positive correlation with adiponectin in both the UC and CD patients. For the first time, the present study demonstrated lower levels of CTRP3 in the UC and CD patients. Decreased serum levels of CTRP3 and its inverse relationship with inflammatory cytokines and TGF‐β levels suggested a possible role for CTRP3 in the pathogenesis of UC and CD diseases.

Coronary artery disease (CAD) is the leading cause of death worldwide. Atherosclerosis, the main underlying cause of CAD, is a progressive inflammatory disease. microRNAs play a substantial role in the inflammatory process and pathogenesis of atherosclerosis. miR-155, a widely studied microRNA, is associated with inflammation but there are conflicting data regarding expression of miR-155 in CAD. miR-10a is also one of the key regulators of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway which have not been evaluated in peripheral blood mononuclear cells (PBMCs) of CAD patients. This is a case-control study conducted on 69 angiography confirmed CAD patients and 65 controls. PBMC expressions of miR-155, miR-10a, interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) were evaluated by real-time PCR in the study population. Also, serum levels of IL-6, TNF-α, interleukin-10 (IL10), and adiponectin were measured by ELISA. No significant differences in miR-155 expression was found between CAD and control group (p = 0.059), while lower expression of miR-10a was observed in CAD individuals compared to controls (p < 0.001). An independent association of miR-10a expression with risk of CAD was also demonstrated. Higher serum levels and PBMC expressions of IL-6 and TNF-α were observed in the CAD group compared to controls (p = 0.002 and p = 0.001). However, serum concentrations of IL-10 and adiponectin were lower in CAD individuals compared to controls (p < 0.001 and p = 0.005, respectively). We found a negative association of miR-10a expression with miR155, TNF-α and IL-6 gene expression as well as serum TNF-α and IL-6 levels. A positive correlation between miR10a and serum IL-10 concentrations was also shown. Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.

Background and purpose: Diclofenac (DF), a widely used non-steroidal anti-inflammatory drug, can induce hepatotoxicity and nephrotoxicity. This study investigated the protective effects of thymoquinone (TQ), a bioactive compound from Nigella sativa, against DF-induced organ damage in rats. Experimental approach: Forty-eight male rats were divided into six groups (8 each) and treated orally for seven days as follows: group 1 (control): normal saline; group 2: DF (50 mg/kg); group 3: DF (50 mg/kg) + silymarin (50 mg/kg); groups 4-6: DF (50 mg/kg) + TQ at 10, 20, or 40 mg/kg, respectively. Serum biochemical parameters, hepatorenal oxidative stress markers, pro-inflammatory cytokines, and apoptosis-related genes were assessed. Histopathological examinations of liver and kidney tissues were also performed. Findings/Results: DF administration induced significant liver and kidney damage, evidenced by elevated serum biochemical markers, increased oxidative stress, inflammation, apoptosis-related gene expression, and histopathological alterations. TQ treatment, particularly at the highest dose (40 mg/kg) effectively attenuated these changes. TQ improved liver and kidney function, reduced oxidative stress markers, suppressed inflammation, modulated apoptosis-related gene expression, and ameliorated histopathological damage. Conclusion and implication: TQ exerted significant protective effects against DF-induced hepatorenal toxicity in rats, potentially through its antioxidant, anti-inflammatory, and anti-apoptotic properties. These findings suggest that TQ may be a promising therapeutic agent for mitigating DF-induced organ damage. However, further research, including clinical trials, is needed to confirm its efficacy and safety in humans.