TUG1 (Taurine Up-Regulated 1)

Taken together, these results may shed light on the possible role of BM-MSC-Exos in regulating apoptosis, cell-cycle progression, and TUG1 expression in leukemic cells. Further studies are warranted to elucidate the molecular mechanisms underlying these effects and to determine how BM-MSC-Exos-mediated modulation of TUG1 might contribute to leukemic cell regulation.

This study demonstrated that SRPK1 inhibition alters lncRNA expression and splicing-related events in PCa. These findings highlight SPHINX31's potential as a therapeutic agent, especially in combination with treatments like Olaparib, necessitating further optimization for selectivity and reduced off-target effects.

Despite their potential as therapeutic targets and diagnostic biomarkers, the clinical application of lncRNAs is limited due to their immunogenicity, delivery challenges, and specificity. By investigating the overall etiology and remaining challenges, we intend to shed light on how modifying lncRNA activity could open up novel treatment avenues for REDs.

In vivo, TUG1 knockdown combined with LEN treatment significantly reduced tumor growth and PD-L1 expression. In conclusion, TUG1 promotes HCC progression by enhancing PD-L1 through miR-377-3p, with its knockdown enhancing the therapeutic efficacy of LEN, highlighting TUG1's potential as a novel target for HCC treatment.

While the study offers significant contributions to the field, there are limitations in its methodology, interpretative depth, and generalizability that merit closer examination. This commentary critically evaluates the findings, suggesting avenues for refinement and further research.

Furthermore, we identified nemo-like kinase, which may change in tandem with TUG1 expression. Our findings indicate the possibility for targeting the TUG1-nemo-like kinase axis as a novel approach for the treatment of HNSCC.

Furthermore, evidence suggests that dysregulation of TUG1 is closely linked to the development and progression of liver diseases. This review explores the key characteristics, mechanisms, and signaling pathways through which TUG1 affects liver disease, offering fresh insights into potential therapeutic directions and new avenues for future TUG1-related research.

We further showed that inhibition of miR-122-5p alleviated the suppression of glycolysis induced by TUG1 depletion. Together, our RNA-seq analysis of TUG1-depleted HCC cells, combined with clinical data, reveals the critical function of TUG1 in promoting glycolysis via sponging miR-122-5p, which is a negative regulator of multiple glycolytic enzymes.

In this study, we systematically evaluate the impact of abnormal TUG1 expression across various diseases, focusing on its mechanisms of action in regulating immune cell infiltration and disease progression in both cancer and non-cancer contexts. We also discuss potential targets for future research related to TUG1's role in these pathogenic processes.

Many of these proteins are known R-loop-associated factors, including DEAD/DEAH-box RNA helicases, poly(ADP-ribose) polymerase 1 (PARP1), and heterogeneous nuclear ribonucleoproteins (HNRNPs), indicating that TUG1 engages R-loop regulatory machinery to maintain genome integrity. Our study provides new insights into lncRNA-mediated R-loop regulation and its role in genome maintenance.

Our data identified a novel molecular pathway comprising the METTL3-m6A-TUG1-miR-9-EIF5A2 signaling axis in HCC, providing new targets for future DOX resistance management.

Additionally, exosomal TUG1 enhanced the polarization of M2 tumor-associated macrophages, which increased the proliferation and metastasis of CHS. Taken together, this study revealed the oncogenic role of TUG1 in CHS and its interactions with the downstream regulatory axis, offering novel insights into the tumorigenic mechanism of CHS.