PVT1 (Pvt1 Oncogene)

Study heterogeneity, variable antibody scoring, and limited assessment of senescence-associated beta-galactosidase and secretory mediators restricted cross-study comparability. Standardized, spatially resolved profiling may refine risk stratification and support senescence-targeted prevention and therapy in keratinocyte cancers.

Further studies are needed to elucidate the functions of this lncRNA in GC. The review protocol was registered on The International Prospective Register of Systematic Reviews (PROSPERO) (CRD42022360864).

Many of deregulated genes were directly bound by all three proteins, suggesting a coordinated transcriptional regulation, revealing a critical axis involving ERα, DOT1L, menin and PVT1. Targeting this RNA-dependent chromatin associated regulatory complex could offer novel therapeutic strategies for BC treatment.

It is important to understand the intricate relationships between PVT1 and different types of human cancers to achieve a better understanding of the disease and treatment options. The current findings identify an upregulated PVT1 as a crucial promoter of the risk of carcinogenesis and tumor metastasis, also dramatically reducing patient survival, underscoring the potential of PVT1 expression as a prognostic marker in cancer.

The quantitative evidence from numerous in vitro and in vivo studies has consistently demonstrated that flavonoid lncRNA modulation leads to a significant reduction in micro vessel density, expression of VEGF, and tumor burden. Improved bioavailability with more advanced nanoformulation and enhancement in preclinical validation of flavonoid lncRNA therapeutics, despite the remaining challenges like limited clinical data and off-target effects, offer low-toxicity targeted means of reprogramming tumor angiogenesis and overcoming resistance to the current therapies.

Exploration of the sequence and structural details of these lncRNA-mRNA interactions led us to an insight on a probable mechanism of a single PVT1 molecule being able to bind multiple mRNAs simultaneously or sequentially, in a spatio-temporal manner. Our research also seeks to further elucidate the contribution of bases and intermolecular interactions in the formation of these complexes.

These findings establish lncRNA PVT1 as a critical epigenetic scaffold coordinating NOP56-E2F1-PPARγ signaling to polarize macrophages toward a pro-tumorigenic M2 phenotype, thereby fueling TNBC aggressiveness. This study unveils novel therapeutic targets for TNBC by disrupting the PVT1-PPARγ axis to rebalance macrophage dynamics and induce tumor-suppressive immunity.

Focusing on the most common ecDNA fusion hotspot, we find that fusion of the 5' end of the long noncoding RNA gene, PVT1-with exon 1 joined to diverse 3' partners-confers increased RNA stability, potentially via an SRSF1-dependent mechanism, and enhances MYC-dependent transcription and cancer cell survival. These results demonstrate that ecDNA fosters genome instability and frequent oncogene fusion formation in cancer.

The combination of cisplatin and metformin (Glucophage) exerts an additive cytotoxic effect and induces apoptosis in NSCLC cells in vitro. This effect is associated with a favorable modulation of key apoptosis-regulating genes and lncRNAs. These findings provide a strong rationale for further mechanistic and preclinical investigation of this combination therapy for lung cancer.

Sex, follicular nodular disease, and Graves' disease were not significant predictors. Our findings suggest an association between fusion-driven thyroid neoplasia and florid CLT, warranting further investigation.