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The long non-coding RNA (lncRNA), GAS5, has garnered significant attention recently for its multifaceted involvement in cellular processes, particularly within the context of diabetes. This comprehensive review delves into the intricate molecular interactions associated with GAS5 and their profound implications for understanding, diagnosing, and effectively managing diabetes mellitus. The article begins by highlighting the global prevalence of diabetes and the urgent need for innovative insights into its underlying mechanisms and therapeutic approaches. It introduces GAS5 as a crucial regulator of gene expression, with emerging significance in the context of diabetes-related processes. The core of this review unravels the regulatory network of GAS5 in diabetes, elucidating its impact on various aspects of the disease. It explores how GAS5 influences insulin signaling pathways, glucose metabolism, and the function of β-cells, shedding light on its role in hyperglycemia and insulin resistance. Moreover, the article underscores the clinical relevance of GAS5's interactions by discussing their associations with different diabetes subtypes, predictive value, and potential applications as both diagnostic tools and therapeutic targets. It provides insights into ongoing research endeavours aimed at harnessing the potential of GAS5 for innovative disease management strategies, including the development of RNA-based therapeutics. Concluding with a forward-looking perspective, the abstract highlights the broader implications of GAS5 in the field of diabetes, such as its connection to diabetic complications and its potential for personalized approaches in disease management. [ABSTRACT FROM AUTHOR]

Novel treatment targets must be discovered to improve the results for patients with prostate cancer, which continues to be a significant worldwide health problem. Growth Arrest-Specific 5 (GAS5) is a long non-coding RNA (lncRNA) that has emerged as a promising target. GAS5 is a non-coding RNA that is a tumour suppressor in many different cancers by reducing cell proliferation and increasing apoptosis. GAS5 influences cell cycle control and apoptosis via interactions with important signalling pathways and microRNAs, as has been shown by recent studies. Furthermore, GAS5 has attracted interest for its diagnostic and prognostic potential in prostate cancer. GAS5 expression is a promising biomarker for disease classification and individualized treatment approaches because of its association with clinicopathological characteristics such as tumour stage, Gleason score, and metastatic potential. Preclinical models have revealed encouraging anticancer benefits from experimental techniques employing GAS5 overexpression or synthetic analogues, indicating the possibility of translational treatments. Whether GAS5 can be used as a diagnostic biomarker and therapeutic target might lead to more effective and individualized ways to fight prostate cancer, improving patient outcomes and quality of life. To utilize its potential for therapy and establish it as a useful addition to the clinical arsenal against this pervasive malignancy, more investigation into the complex molecular pathways of GAS5 in prostate cancer is essential. This review highlights the recent advancements and insights into the role of GAS5 in prostate cancer pathogenesis and progression. [ABSTRACT FROM AUTHOR]

Pituitary adenomas are slow-growing tumors originated from the anterior part of pituitary gland. These tumors are associated with dysregulation of a number of long non-coding RNAs (lncRNAs). PVT1, TUG1, MALAT1, NEAT1 and GAS5 are among lncRNAs with important roles in the regulation of cell proliferation, cell apoptosis, cell differentiation and cell cycle transition. In the current study, we assessed expression levels of PVT1, TUG1, MALAT1, NEAT1 and GAS5 in the pituitary adenoma samples compared with adjacent non-cancerous samples to find their relevance with this type of tumors and their potential as diagnostic markers in these tumors. Expression of NEAT1 was significantly higher in total adenoma tissues (Expression ratio (95% CI)= 7.06 (2.31–21.4), P value= 0.02) and in non-functioning pituitary adenoma (NFPA) samples (Expression ratio (95% CI)= 8.5 (2.17–33.12), P value= 0.04) compared with corresponding controls. Although both lncRNAs had appropriate sensitivity values for discrimination of NFPAs from adjacent non-cancerous tissues (0.84 and 0.90 for PVT1 and NEAT1, respectively), the calculated AUC values were not adequate for either lncRNAs (0.63 ± 0.04 and 0.58 ± 0.04 for PVT1 and NEAT1, respectively). Therefore, NEAT1 and PVT1 lncRNAs are dysregulated in NFPA. The current study suggests the role of NEAT1 and PVT1 in the pathogenesis of NFPA. [ABSTRACT FROM AUTHOR]

LncRNAs, or long non-coding RNAs, are a subset of RNAs that play a regulatory role in a wide range of biological functions, including RNA processing, epigenetic regulation, and signal transduction. Recent research indicates that lncRNAs play a key role in the development and spread of cancer by being dysregulated in the disease. In addition, lncRNAs have been linked to the overexpression of certain proteins that are involved in tumor development and progression. Resveratrol has anti-inflammatory and anti-cancer properties that it exerts through regulating different lncRNAs. By the regulation of tumor-supportive and tumor-suppressive lncRNAs, resveratrol acts as an anti-cancer agent. By downregulating the tumor-supportive lncRNAs DANCR, MALAT1, CCAT1, CRNDE, HOTAIR, PCAT1, PVT1, SNHG16, AK001796, DIO3OS, GAS5 and H19, and upregulating MEG3, PTTG3P, BISPR, PCAT29, GAS5, LOC146880, HOTAIR, PCA3, NBR2, this herbal remedy causes apoptosis and cytotoxicity. For the purpose of using polyphenols in cancer therapy, it would be helpful to have more in-depth knowledge about lncRNA modulation via resveratrol. Here, we discuss the current knowledge and future promise of resveratrol as modulators of lncRNAs in different cancers. [ABSTRACT FROM AUTHOR]

Long non coding RNAs (lncRNAs) are involved in the tumor growth, invasion, metastasis, and cancer recurrence. The improper expression of certain lncRNAs is correlated with the prognosis of the cancer patients. LncRNA single nucleotide polymorphisms (SNPs) largely affect the expression, structure, and function of lncRNAs. Therefore, they affect cancer prognosis and susceptibility. In the present review, we tried to collect all published papers on the prognostic ability in cancer considering the correlation of different lncRNAs polymorphism and survival. We explored the association between lncRNA (i.e. MALAT1, ANRIL, GAS5, TP73-AS1, HOTAIR, H19, LncARSR, PVT1, HOTTIP, PRNCR1, PCAT1, CASC8, UCA1, SNHG5, PARP1, Linc00312, and NEAT) polymorphisms with cancer prognosis. The HOTAIR rs920778/rs4759314 and MALAT1 rs664589 polymorphisms play an important role in cancer relevant functions. Other lncRNAs polymorphisms are special for certain kinds of cancer, indicating their function in specific signaling pathways. Accordingly, the individual or combined genotypes of lncRNA polymorphisms are able to predict cancer prognosis. However, most of the samples are Chinese and do not represent the global population. More large-scale trials of different ethnic groups as well as comprehensive health records are therefore needed for more validation of the results. [ABSTRACT FROM AUTHOR]

N6-Methyladenosine (m6A) RNA methylation is the most prevalent post-transcriptional modification mechanism in humans and plays an important role in the pathogenesis of various tumors. However, the investigation of m6A modification in Esophageal squamous cell carcinoma (ESCC) remains in its infancy. Transcriptome-wide m6A changes were profiled using human m6A epitranscriptomic microarrays in ESCC tissues and adjacent normal tissues. Differentially m6A-methylated mRNAs, lncRNAs and Mid-size ncRNAs were identified, followed by functional enrichment analysis. Moreover, we also establish a competing endogenous RNA (ceRNA) network based on the m6A-related lncRNA growth arrest specific 5 (GAS5) specific transcript（NR_152533）. The results suggested that RALYL may be a target gene for miR-3912–5p, and that GAS5 regulated RALYL expression by binding to miR-3912–5p. [ABSTRACT FROM AUTHOR]

Dysregulation of the long noncoding RNA GAS5 in human cancer has been identified in recent studies. In this study, we confirmed a negative correlation between the GAS5 expression level and papillary thyroid carcinoma clinicopathologic characteristics, such as the tumor size, lymph node metastasis, the TNM stage and BRAFV600E mutation. The viability and metastasis of papillary thyroid carcinoma cells were detected by CCK-8 and transwell assays, respectively. The results showed that upregulation of GAS5 significantly inhibited papillary thyroid cancer cell growth, migration and invasion in vitro. RNA transcriptome sequencing was performed to explore the underlying targets of GAS5. Through qRT-PCR and Western blot analysis, we found that ectopic expression of GAS5 significantly increased IFI44 and STAT1 levels. Taken together, these findings suggest that GAS5 is a tumor suppressor in papillary thyroid carcinoma, and the action of GAS5 may be mediated through the IFNγ/STAT1 signaling pathway. [ABSTRACT FROM AUTHOR]