GAS5 (Growth Arrest Specific 5)

The variant rs145204276 was considered for the first time in AML; however, no significant clinical associations or transcriptional effects were found. Taken together, our findings provide evidence that the rs55829688 promoter variant reduces GAS5 expression in AML and could potentially be a prognostic marker.

It also enhanced the sensitivity of cell lines to paclitaxel, decreased the spheroid formation and modulated the expressions of EMT markers. These cumulative findings revealed that EPA exhibits anti-cancer activity against pancreatic cancer.

Nonetheless, the study has limitations, including reliance on a single cell line and the assessment of direct apoptosis only. These findings highlight a complex interplay between GAS5, CD20, rituximab, and cellular pathways, underscoring the significance of understanding these interactions to enhance cancer therapy outcomes.

Functional assays demonstrated that this regulatory circuit modulates TC cell proliferation, invasion, and metastasis in vitro and in vivo, with GAS5 acting for miR-128-3p to regulate CDKN2A expression. These findings provide a comprehensive systems-level perspective on cuproptosis-related mechanisms in TC and highlight the therapeutic promise of targeting the cuproptosis pathway and its regulatory networks in thyroid cancer management.

Functionally, GOLGA8B was shown to activate the STAT3 signaling pathway.GAS5 inhibits STAT3 phosphorylation by downregulating GOLGA8B, thereby inducing cell apoptosis.In vivo animal experiments confirmed that GAS5 overexpression suppresses tumor growth.In vivo animal experiments confirmed that GAS5 overexpression suppresses tumor growth. In summary, this study reveals that GAS5 regulates ovarian cancer cell apoptosis by modulating the O-GlcNAcylation of GOLGA8B, which in turn affects the STAT3 signaling pathway, providing a new potential therapeutic target for ovarian cancer.

WTAP epitranscriptomically regulates VSMC ferroptosis via the GAS5/EZH2/IRF4/FTH1 axis, revealing a novel mechanism in vascular restenosis pathogenesis and a potential therapeutic target. Antioxid. Redox Signal. 00, 000-000.

Bioinformatic analyses identified correlations between these lncRNAs and crucial genes involved in cell survival, migration, and angiogenesis, emphasizing possible lncRNA-miRNA-mRNA regulatory axes. The cardamom nanoemulsion demonstrates enhanced anticancer activity relative to the crude extract and could represent a novel therapeutic approach for colorectal cancer by modulating lncRNAs and related molecular pathways.

These articles have been retracted. The Publisher apologizes for any inconvenience this may cause.

Thus, GPRC5B is directly bound to miR-12. GAS5 promotes proliferation, migration, and invasion of prostate cancer cells and participates in malignant progression of tumors by suppressing miR-12-mediated regulation of GPRC5B expression.

These insights into lncRNA-mediated regulatory mechanisms provide promising therapeutic targets for RCC, suggesting that modulating specific lncRNAs or their associated pathways could offer innovative strategies for treatment and prognosis. This review presents a comprehensive analysis of the biogenesis, functions, and regulatory roles of lncRNAs in RCC, emphasizing their potential as diagnostic biomarkers and therapeutic targets to improve patient outcomes.

PKMYT1 and GAS5 demonstrated strong diagnostic value in distinguishing high-aggressive from low-aggressive tumors, while circMET showed notable diagnostic efficacy in differentiating low-aggressive PTC tumors from adjacent normal tissues. Furthermore, GAS5 expression levels were correlated with blood calcium levels.

This study highlights the potential prognostic significance of the epigenetic regulation of ADIPOQ in TNBC. The in silico findings shed light on the molecular pathways associated with TNBC progression and warrant further investigation to validate their role in clinical outcomes and underlying biological mechanisms.