Circulating microRNAs as diagnostic and therapeutic biomarkers in gastric and esophageal cancers.

Gastric and esophageal cancers are as main cancers of the gastrointestinal (GI) tract, which are associated with poor diagnosis and survival. Several efforts were made in the past few decades to finding effective therapeutic approaches, but these approaches had several problems. Finding new biomarkers is a critical step in finding new approaches for the treatment of these cancers. Finding new biomarkers that cover various aspects of the diseases could provide a choice of suitable therapies and better monitoring of patients with these cancers. Among several biomarkers tissue specific and circulating microRNAs (miRNAs) have emerged as powerful candidates in the diagnosis of gastric and esophageal cancers. MiRNAs are small noncoding single-stranded RNA molecules that are found in the blood and regulate gene expression. These have numerous characteristics that make them suitable for being used as ideal biomarkers in cancer diagnosis. Research has indicated that the level and profile of miRNA in serum and plasma are very high. They are potentially noninvasive and sensitive enough to detect tumors in their primary stages of infection. Multiple lines of evidence indicate that the presence, absence, or deregulation of several circulating miRNAs (i.e., let-7a, miR-21, miR-93, miR-192a, miR-18a, and miR-10b for gastric cancer, and miR-21, miR-375, miR-25-3p, miR-151a-3p, and miR-100-3p for esophageal cancer) are associated with initiation and progression of gastric and esophageal cancers. The aim of this review is to highlight the recent advances in the roles of miRNAs in diagnosis and treatment of gastric and esophageal cancers.

Serum Levels of Long Non-coding RNAs NEAT1, GAS5, and GAPLINC Altered in Rheumatoid Arthritis.

BACKGROUND: Rheumatoid arthritis (RA), an autoimmune joint inflammatory disease, presents a significant challenge due to its prevalence, particularly among women, affecting around 6% of individuals over the age of 65. Novel insights into disease mechanisms are crucial for improved diagnostic and therapeutic approaches. OBJECTIVE: Long non-coding RNAs (lncRNAs) have emerged as potential contributors to the pathogenesis of various autoimmune diseases, including RA. This study aims to investigate the unique roles of four lncRNAs-NEAT1, GAS5, TMEVPG1, and GAPLINC-in the etiology of RA. METHODS: Leveraging isolated serum samples from RA patients and healthy controls, we comprehensively evaluated the expression profiles of these lncRNAs. RESULTS: Notably, our findings unveil a distinctive landscape of lncRNA expressions in RA. Among them, GAPLINC exhibited a significantly elevated average expression in the serum samples of RA patients, suggesting a potential biomarker candidate for disease stratification. Importantly, reduced expression of NEAT1 and GAS5 was observed in RA patients, highlighting their possible roles as diagnostic and prognostic markers. Conversely, TMEVPG1 displayed unaltered expression levels in RA samples. CONCLUSION: Our study introduces a novel dimension to RA research by identifying NEAT1, GAS5, and GAPLINC as promising serological biomarkers. These findings hold significant clinical implications, offering potential avenues for improved diagnosis, disease monitoring, and therapeutic interventions in RA.

miRNA-21, an Important Regulator of Autoimmune Diseases.

miRNA-21 is regarded as both an abundant and highly conserved member of the microRNA (miRNA) family. It is expressed in virtually every cell and is responsible for critical regulatory actions that are important in health and disease. This microRNA has been shown to potentially have a role in the pathogenesis of several immune-related disorders, including autoimmune diseases, such as Multiple sclerosis and systemic lupus erythematosus, as two prominent examples of diseases that might be involved. In the current research, we looked at the role of miRNA-21, regarded as one of the most significant pathogenic miRNAs with a role in the development of autoimmune illness.

The critical role and functional mechanism of microRNA-146a in doxorubicin-induced apoptosis in breast cancer cells.

BACKGROUND: Breast cancer among women is the most frequently diagnosed cancer and the leading cause of death worldwide. There many advances in diagnosing and treating this disease, early diagnosis and treatment are still a significant challenge in the early stages. In recent years, microRNAs have attracted much attention in cancer diagnosis and treatment. However, the role of miR-146a in breast cancer is still controversial. We aimed to investigate the roles of miR-146a in apoptosis in breast cancer cells. METHODS: A microarray dataset from the GEO database was selected, and using the GEO2R tool, the gene expression profile of this dataset was extracted. Then, the target scan database was used to explore the miR-146a target genes. The link between the signaling pathways was collected. We used miR-146a mimic, which was transfected to the MCF-7 cells to investigate the miR-146a roles in the apoptosis. The expression levels of miR-146a and BAX, BCL-2, and p-21(most essential genes in the apoptosis) were quantified by qPCR and western blot analysis. RESULTS: Our findings indicated that doxorubicin induces miR-146a expression. In addition, overexpression of miR-146a affected MCF-7 cell viability, induced apoptosis, and led to reduced expression levels of BCL-2 and P-21, as well as increased BAX expression levels. CONCLUSION: Considering the role of doxorubicin in inducing apoptosis and increasing the expression of miR-146a, it can be suggested that this miR is involved in inducing apoptosis in BC cells. In addition, miR-146a can be considered a therapeutic candidate.

Rheumatoid arthritis and non-coding RNAs; how to trigger inflammation.

Rheumatoid arthritis (RA) is a systemic and chronic inflammatory disease categorized by continuous synovitis in the joints and systemic inflammatory responses that can cause lifelong disability. The major cause of RA is the dysregulation of the immune response. The development of RA disease includes multiplex association of several interleukins and cells, which leads to synovial cell growth, cartilage and bone damage. The primary stage of RA disease is related to the modification of both the innate and adaptive immune systems, which leads to the formation of autoantibodies. This process results in many damaged molecules and epitope spreading. Both the innate (e.g., dendritic cells, macrophages, and neutrophils) and acquired immune cells (e.g., T and B lymphocytes) will increase and continue the chronic inflammatory condition in the next stages of the RA disease. In recent years, non-coding RNAs have been proved as significant controllers of biological functions, especially immune cell expansion and reactions. Non-coding RNAs were primarily containing microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA). Various studies confirmed non-coding RNAs as hopeful markers for diagnosing and curing RA. This review will describe and cover existing knowledge about RA pathogenesis, which might be favorable for discovering possible ncRNA markers for RA.