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Objective: Gastric cancer (GC) is an exceedingly prevalent cancer worldwide and one of the main reasons for death from cancer. The individuals’ susceptibility to GC depends upon several genetic and epigenetic alterations that occur over their lifetime. The C-FOS is an oncoprotein that engages in tumorigenesis through its oncogenic roles. It modulates many cellular functions, and its aberrant expression can lead to several types of cancers. Materials and Methods: The Amplification Refractory Mutation System (ARMS) PCR technique was conducted to detect genotypic types of rs997415225 in 50 healthy controls and 45 patients with GC. Furthermore, the quantitative Real-Time PCR (qRT-PCR) technique was applied to determine C-FOS relative gene expression in 20 healthy controls and 20 cancer patients. Results: Genotypic types of rs997415225 did not seem to be correlated with GC (P > 0.05), but allele “A” frequency was correlated (P = 0.048). Also, there was a significant difference between the two groups regarding the C-FOS gene expression level (P = 0.044). Conclusions: It has been found that genotypic types of rs997415225 have no impact on GC; however, the presence of allele “A” is associated with a potential risk of GC development. In addition, the increased C-FOS gene expression was linked to the progression of this cancer; hence, preventing GC through C-FOS down-regulation might be a promising approach.

Background: Non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), play critical roles in the pathogenesis and progression of pulmonary artery hypertension (PAH). LncRNA H19, myocardial infarction-associated transcript (MIAT), miR-29a, and miR-33a have been suggested as potential targets for treating arterial hypertension. We explored the expression pattern of non-coding RNAs H19, MIAT, miR-29a, and miR-33a in monocrotaline (MCT)-induced PAH rats. Moreover, we investigated whether perillyl alcohol (PA) and quercetin (QS), two plant derivatives with beneficial effects on PAH-induced abnormalities, act through regulating the expression of these non-coding RNAs. Methods: Male Wistar rats (n = 30) were divided into five groups. MCT (60 mg/kg) was injected subcutaneously to induce PAH. PA (50 mg/kg daily) and QS (30 mg/kg daily) were administered three weeks after induction of PAH. H&E staining and qRT-PCR were performed to assess arteriole wall thickness and gene expression, respectively. Results: Right ventricular systolic pressure (RVSP) and right ventricular hypertrophy (RVH) increased in MCT and MCT + Veh. groups compared to the control group (in both P