SRSF9 mediates oncogenic RNA splicing of SLC37A4 via liquid-liquid phase separation to promote oral cancer progression.

Introduction: Oral cancer represents a significant proportion of head and neck malignancies, accounting for approximately 3 % of all malignant tumors worldwide.

Objectives: Alternative splicing (AS), a post-transcriptional regulatory mechanism, is increasingly linked to cancer development. The precise impact of AS on oral cancer progression is not well understood.

Noncoding RNA-encoded peptides in cancer: biological functions, posttranslational modifications and therapeutic potential.

In the present era, noncoding RNAs (ncRNAs) have become a subject of considerable scientific interest, with peptides encoded by ncRNAs representing a particularly promising avenue of investigation. The identification of ncRNA-encoded peptides in human cancers is increasing. These peptides regulate cancer progression through multiple molecular mechanisms.

Long non‑coding RNA ABHD11‑AS1 inhibits colorectal cancer progression through interacting with EGFR to suppress the EGFR/ERK signaling pathway.

Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinformatic analysis, reverse transcription‑quantitative PCR and hybridization revealed that ABHD11‑AS1 expression was decreased in CRC samples and associated with an unfavorable prognosis.

CircRNF13 enhances IGF2BP1 phase separation-mediated ITGB1 mRNA stabilization in an m6A-dependent manner to promote oral cancer cisplatin chemoresistance.

Oral cancer ranks among the most common malignancies within the head and neck region; however, its etiology remains inadequately understood despite substantial research advances in recent years. Many studies highlight the regulatory role of circular RNAs (circRNAs) in human cancers, suggesting their potential as cancer biomarkers. However, their specific mechanisms in oral cancer are not well understood.

Diallyl disulfide induces DNA damage and growth inhibition in colorectal cancer cells by promoting POU2F1 ubiquitination.

Previous studies have demonstrated that diallyl disulfide (DADS) exhibits potent anti-tumor activity. However, the pharmacological actions of DADS in inhibiting the growth of colorectal cancer (CRC) cells have not been clarified. Herein, we show that DADS treatment impairs the activation of the pentose phosphate pathway (PPP) to decrease PRPP (5-phosphate ribose-1-pyrophosphate) production, enhancing DNA damage and cell apoptosis, and inhibiting the growth of CRC cells.

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling During Neurodevelopment.

Intellectual disability (ID) is a condition characterized by cognitive impairment and difficulties in adaptive functioning. In our research, we identified two de novo mutations (c.955C>T and c.

Alternative splicing in mouse brains affected by psychological stress is enriched in the signaling, neural transmission and blood-brain barrier pathways.

Psychological stress increases the risk of major psychiatric disorders. Psychological stress on mice was reported to induce differential gene expression (DEG) in mice brain regions. Alternative splicing is a fundamental aspect of gene expression and has been associated with psychiatric disorders but has not been investigated in the stressed brain yet.

Changes of immune-related factors in the blood of schizophrenia and bipolar disorder patients receiving monotherapy.

Schizophrenia (SCZ) and bipolar disorder (BPD) are associated with abnormal expression of immune-related factors (IRFs), which have been proposed as biomarkers of either disease diagnosis (trait markers) or treatment (state markers). However, the state markers have been found to be less reproducible than the trait markers in previous studies. In the current study, we focused on the changes of IRFs in blood of SCZ and BPD patients receiving monotherapy.

Glioma cells are resistant to inflammation‑induced alterations of mitochondrial dynamics.

Accumulating evidence suggests that inflammation is present in solid tumors. However, it is poorly understood whether inflammation exists in glioma and how it affects the metabolic signature of glioma. By analyzing immunohistochemical data and gene expression data downloaded from bioinformatic datasets, the present study revealed an accumulation of inflammatory cells in glioma, activation of microglia, upregulation of proinflammatory factors (including IL‑6, IL‑8, hypoxia‑inducible factor‑1α, STAT3, NF‑κB1 and NF‑κB2), destruction of mitochondrial structure and altered expression levels of electron transfer chain complexes and metabolic enzymes.

Integrative analyses prioritize GNL3 as a risk gene for bipolar disorder.

Genome-wide association studies (GWASs) have identified numerous single nucleotide polymorphisms (SNPs) associated with bipolar disorder (BD), but what the causal variants are and how they contribute to BD is largely unknown. In this study, we used FUMA, a GWAS annotation tool, to pinpoint potential causal variants and genes from the latest BD GWAS findings, and performed integrative analyses, including brain expression quantitative trait loci (eQTL), gene coexpression network, differential gene expression, protein-protein interaction, and brain intermediate phenotype association analysis to identify the functions of a prioritized gene and its connection to BD. Convergent lines of evidence prioritized protein-coding gene G Protein Nucleolar 3 (GNL3) as a BD risk gene, with integrative analyses revealing GNL3's roles in cell proliferation, neuronal functions, and brain phenotypes.