HULC (Hepatocellular Carcinoma Up-Regulated Long Non-Coding RNA)

These findings reveal a TMAO-HULC signaling axis that positively influences the levels of oncogenic miRNAs. However, since a single cell line model was used in this study, it needs for further investigation across diverse CRC cell lines to confirm its generalizability.

In addition, we also discuss the potential of lncRNAs as therapeutic targets for HCC, such as: lncRNA MIR31HG, CASC2c, and lncRNA AC115619. Furthermore, we also explore the application prospects of lncRNAs as potential biomarkers and therapeutic targets, providing new perspectives and directions for future HCC research.

This review comprehensively summarizes recent advances in understanding the biological roles, molecular mechanisms, and clinical implications of HULC in digestive system cancers. Furthermore, we discuss its potential as a novel diagnostic biomarker and therapeutic target, providing insights into precision medicine strategies for gastrointestinal malignancies.

This study found that plasma lncRNAs HULC and RP11-731F5.2 are potential biomarkers for HCC risk, while RP11-731F5.2 and KCNQ1OT1 may serve as noninvasive biomarkers for liver damage due to HCV infection. These findings highlight the potential of lncRNAs in enhancing early diagnosis and monitoring of HCC in CHC patients.

In conclusion, the results of this study provide evidence of the TMAO/HULC/P38MAPK axis involvement in the pathogenesis of MAFLD by increasing the expression of genes involved in inflammation and fibrosis. Our data suggests that TMAO reduction could be a therapeutic target in MAFLD through gut microbiome modulation.

Moreover, targeting these lncRNAs may lead to innovative therapeutic strategies aimed at disrupting tumor-supportive inflammatory cascades and restoring an effective antitumor immune response. Understanding the intricate interplay between lncRNA-mediated epigenetic regulation and macrophage polarization not only refines our grasp of HCC progression but also opens new pathways for interventions designed to improve patient outcomes.

Combination of transcript levels of CASP2, CASP8, BCL2, HULC and PVT1 changed AUC to 0.84 and 0.72 in tissues and blood samples, respectively. To conclude, these genes might be regarded as putative contributors in the pathophysiology of periodontitis.

HULC promotes CRC cell proliferation, migration, and EMT through its interaction with IGF2BP2, highlighting the critical role of the HULC-IGF2BP2 axis in CRC progression. These findings identify HULC as a potential molecular target for CRC treatment and offer new insights for therapeutic strategies targeting CRC patients.

In recent years, it has been shown that dysregulation of molecular mechanisms in many LncRNAs such as MIR22HG, HULC, AGAP2-AS1, MALAT1, PVT1, TTTY14, HOTAIRM1, PTAR, LPP-AS2, LINC00336, and TINCR are connected with the GBM. Therefore, this scientific review paper focused on the molecular mechanisms of these LncRNAs in the context of GBM.

These lncRNAs include SNHG15, HULC, HCP5, MT1JP, LncMat2B, DLX6-ASL, Linc00665, CARMN, and Lnc-EinRP44-3:6. These lncRNAs have been shown to target microRNAs and mRNAs and modulate the expression of genes involved in cisplatin resistance, which is important in treating breast cancer.

Despite indistinguishable heritability estimates between the melanoma classifications, PRS suggest germline genetics may influence whether a person gets in situ melanoma or invasive melanoma. PRS could potentially help stratify populations based on invasive melanoma risk, informing future screening programs without exacerbating the current burden of melanoma overdiagnosis.