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Elucidating the mechanisms underlying cancer development and proliferation is important for the development of therapeutic methods for the complete cure of cancer. In particular, the identification of diagnostic markers for early detection and new therapeutic strategies for refractory gastrointestinal cancers are needed. Various abnormal phenomena occur in cancer cells, such as functional changes of proteins, led by genomic mutations, and changes in gene expression due to dysregulation of epigenetic regulation. This is no exception for noncoding RNA (ncRNA), which do not encode proteins. Recent reports have revealed that microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA) are deeply involved in cancer progression. These ncRNAs have attracted attention as gene expression regulatory molecules. Recent advances in technology have made it possible not only to read DNA and RNA sequences but also to study the modification state of each base. In particular, comprehensive analysis of N6-methyladenosine (mA) has been performed by many research groups, with multiple studies reporting that mA modifications of specific genes are associated with cancer progression. Based on the above, this review examines how ncRNA modifications are related to cancer progression in gastrointestinal cancers such as colorectal and pancreatic cancer. We also discuss enzyme inhibitors that have been reported to have drug discovery potential targeting mA modifications. By utilizing the new perspective of ncRNA modification, we may be able to accumulate knowledge on the molecular biology of cancer and contribute to human health through diagnosis and treatment.
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http://dx.doi.org/10.1111/cas.16380 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
September 2025
University Sousse, Faculty of Medicine "Ibn El-Jazzar", Department of Medical Genetics, Sousse, Tunisia.
The global epidemic of overweight and obesity is closely linked to the development of chronic kidney disease (CKD), with extremely obese individuals facing a particularly high risk. This study aimed to assess the relationship between lipid profile levels, SIRT1 expression, and RNA-34a-5P in the regulation of blood lipid levels among severely obese individuals with renal diseases. Conducted over six months in three specialized hospitals, the study included 100 participants divided into two groups: 50 obese individuals with renal diseases and 50 obese controls without renal problems.
View Article and Find Full Text PDFCell Mol Life Sci
September 2025
Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
View Article and Find Full Text PDFJ Virol
September 2025
Division of Pediatric Infectious Disease, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Rift Valley fever virus (RVFV) causes mild to severe disease in livestock and humans. It was first identified in 1931 during an epizootic in Kenya and has spread across Africa and into the Middle East. Hematopoietic cells are one of the major targets of RVFV ; however, their contribution to RVFV pathogenesis remains poorly understood.
View Article and Find Full Text PDFmSphere
September 2025
Department of Biology, Johns Hopkins University, Baltimore, Maryland, USA.
Oxidative stress induces a wide range of cellular damage, often causing disease and cell death. While many organisms are susceptible to the effects of oxidative stress, haloarchaea have adapted to be highly resistant. Several aspects of the haloarchaeal oxidative stress response have been characterized; however, little is known about the impacts of oxidative stress at the translation level.
View Article and Find Full Text PDFRecursive splice sites are rare motifs postulated to facilitate splicing across massive introns and shape isoform diversity, especially for long, brain-expressed genes. The necessity of this unique mechanism remains unsubstantiated, as does the role of recursive splicing (RS) in human disease. From analyses of rare copy number variants (CNVs) from almost one million individuals, we previously identified large, heterozygous deletions eliminating an RS site (RS1) in the first intron of that conferred substantial risk for attention deficit hyperactivity disorder (ADHD) and other neurobehavioral traits.
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