mei ahmed

Glioblastoma (GBM) is a highly aggressive and treatment-resistant brain tumor. Recent advancements have highlighted the crucial role of long noncoding RNAs (lncRNAs) in GBM's molecular biology. Unlike protein-coding RNAs, lncRNAs regulate gene expression through transcription, post-transcriptional modifications, and chromatin remodeling. Some lncRNAs, like HOTAIR, CCAT2, CRNDE, and MALAT1, promote GBM development by affecting tumor suppressors and various signaling pathways like PI3K/Akt, mTOR, EGFR, NF-κB, and Wnt/β-catenin. Conversely, certain lncRNAs such as TUG1, MEG3, and GAS8-AS1 act as tumor suppressors and are associated with better prognosis. The study presented in the manuscript aims to explore the involvement of lncRNAs in GBM, focusing on their roles in tumor progression, proliferation, invasion, and potential implications for early detection and immunotherapy. The research seeks to elucidate the mechanisms by which specific lncRNAs influence GBM characteristics and highlight their potential as therapeutic targets or biomarkers in managing this aggressive form of brain cancer.

Prostate cancer (PC) ranks among the most prevalent cancers in males. Recent studies have highlighted intricate connections between long non-coding RNAs (lncRNAs), natural products, and cellular signaling in PC development. LncRNAs, which are RNA transcripts without protein-coding function, influence cell growth, programmed cell death, metastasis, and resistance to treatments through pathways like PI3K/AKT, WNT/β-catenin, and androgen receptor signaling. Certain lncRNAs, including HOTAIR and PCA3, are associated with PC progression, with potential as diagnostic markers. Natural compounds, such as curcumin and resveratrol, demonstrate anticancer effects by targeting these pathways, reducing tumor growth, and modulating lncRNA expression. For instance, curcumin suppresses HOTAIR levels, hindering PC cell proliferation and invasion. The interaction between lncRNAs and natural compounds may open new avenues for therapy, as these substances can simultaneously impact multiple signaling pathways. These complex interactions offer promising directions for developing innovative PC treatments, enhancing diagnostics, and identifying new biomarkers for improved prevention and targeted therapy. This review aims to map the multifaceted relationship among natural products, lncRNAs, and signaling pathways in PC pathogenesis, focusing on key pathways such as AR, PI3K/AKT/mTOR, WNT/β-catenin, and MAPK, which are crucial in PC progression and therapy resistance. Regulation of these pathways by natural products and lncRNAs could lead to new insights into biomarker identification, preventive measures, and targeted PC therapies.

Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality globally, largely attributable to its molecular heterogeneity and resistance to current therapeutic modalities. Dysregulation of key intracellular signaling pathways, including EGFR, PI3K/AKT/mTOR, JAK/STAT, and p53, plays a central role in NSCLC pathogenesis, driving tumor initiation, progression, metastasis, and therapeutic resistance. Increasing evidence highlights long non-coding RNAs (lncRNAs) as critical regulatory molecules within these signaling networks. Aberrant lncRNA expression contributes to oncogenic signaling, modulates the tumor microenvironment, and promotes hallmark cancer traits such as uncontrolled proliferation, evasion of apoptosis, metastasis, and chemoresistance. This review synthesizes contemporary findings on the molecular mechanisms by which lncRNAs influence major oncogenic cascades in NSCLC. Both oncogenic and tumor-suppressive lncRNAs are examined, with an emphasis on their functional interplay with signaling mediators and their contributions to tumor biology. Moreover, the clinical relevance of lncRNAs as diagnostic and prognostic biomarkers is explored, alongside emerging therapeutic strategies designed to target lncRNA-mediated dysregulation. Approaches such as antisense oligonucleotides, RNA interference, and CRISPR/Cas9-based gene modulation offer promising avenues for therapeutic intervention. This review provides a comprehensive framework for understanding the roles of lncRNAs in NSCLC and supports the advancement of lncRNA-targeted precision medicine strategies in lung cancer management.

Multiple sclerosis (MS) is an autoimmune disease associated with neurological impairments. The study aimed to evaluate the role of the noncoding RNAs THRIL/miR-137 in MS pathogenesis via studying their effect on the immunological transcriptional loop STAT4/STAT6/GATA3, and their association with MS-related neurological impairments and disease subtypes. Overall, 148 participants were included: 74 MS patients and 74 matched healthy controls. Gene expressions of THRIL, miR-137, STAT4, STAT6, and GATA3 were assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). The potential protein interaction networks of these genes were predicted using bioinformatic analysis. Compared with the control group, THRIL, STAT4, and GATA3 were upregulated, whereas miR-137 and STAT6 were downregulated in MS patients. Furthermore, THRIL, STAT4, and GATA3 were upregulated, while miR-137 and STAT6 were downregulated in MS patients with Expanded Disability Status Scale (EDSS) ≥ 3.5, relative to patients with EDSS < 3.5. Similarly, THRIL, STAT4, and GATA3 were upregulated, while miR-137 and STAT6 were downregulated in Secondary Progressive MS (SPMS) patients relative to Relapsing-Remitting MS (RRMS). Notably, receiver operating characteristic (ROC) curve analysis revealed that THRIL, miR-137, and STAT4/STAT6/GATA3 can be used in differentiating between MS patients with neurological impairments as well as MS subtypes. Significantly, logistic analysis revealed that THRIL, miR-137, and STAT4/STAT6/GATA3 could act as predictors to diagnose MS and the associated neurological impairments. In conclusion, the study demonstrated for the first time the role of THRIL/miR-137 in regulating the immunological transcriptional loop STAT4/STAT6/GATA3, which may contribute to neurological complications. These findings provide insights into MS pathogenesis and highlight the potential of these genes as biomarkers or therapeutic targets.