DGCR5 (DiGeorge Syndrome Critical Region Gene 5)

They have the potential to serve as novel biomarkers as they are detectable in bodily fluids and tissues. These findings enhance gallbladder treatments, mitigating resistance to chemo- and radiotherapy.

While some studies on the uses of DGCR5 have been carried out, the small sample size makes them unreliable. In this review, we presented a compilation of recent publications addressing the potential of lncRNA DGCR5 that could be considered as biomarkers or therapeutic targets, with the hopes of providing promised implications for future cancer therapy.

The low expression of ADAM12 may weaken the digestion of extracellular matrix (ECM) molecules, which can result in the invasion and metastasis of tumor cells. This occurs without the catalysis of ECM proteases, thereby impacting the invasion and metastasis of gastric cancer cells. Additionally, the analysis of immune infiltration suggests that ADAM12 and PDGFRB may influence changes in the tumor immune microenvironment, thereby affecting the occurrence and development of gastric cancer. This study contributes to a deeper understanding of the role of the matrine-related ceRNA network in gastric cancer, providing a reference for clinical diagnosis and treatment. It holds significant importance in discovering new drug treatment targets.

Our analysis observed that the MES transition is regulated by complex interplays between the signalling pathways and EMT factors. Nevertheless, further empirical studies are required to elucidate the complexity in this process between these EMT factors and the signalling involved in the GBM MES transition.

A series of bioinformatic and molecular biological assays unveiled that hsa_circ_0047880 was positively associated with the development of GC. Conclusions The ncRNA-based serum exosome cd-score for the prediction and early diagnosis of GC provides a promising liquid biopsy strategy for personalized medicine.

These findings provide novel insights into understanding the interactions of m6A methylation regulation and tumor stemness on LGG development and contribute to guiding more precise immunotherapy strategies.

Importantly, synthetic splice-switching oligonucleotides (SSOs) disrupt the splicing switch of DGCR5 and potently suppress ESCC tumor growth. These findings uncover the mechanism for Wnt signaling in lncRNA splicing and suggest that the DGCR5 splicing switch may be a targetable vulnerability in ESCC.

A significant dysregulation of lncRNAs was previously observed in GBM compared to non-tumor controls using both transcriptome sequencing and RT‑qPCR and was newly confirmed also by analyzing the TCGA-GBM dataset. We also showed possible effect of LINC00634 upregulation on the growth pattern of U251-derived GBM tumors in vivo. Our study shows that lncRNAs are dysregulated in GBM and could, therefore, serve as promising diagnostic biomarkers in GBM as well as potential therapeutic targets.

Finally, in vivo experiments were utilized to validate that knockdown of DGCR5 suppressed the Warburg effect via targeting of the miR-195/HK2 axis to increase the radio-sensitivity of ESCC. Our study reveals that down-regulation of DGCR5 resulted in inhibition of the Warburg effect through interaction with the miR-195/HK2 axis increasing ESCC cell apoptosis after irradiation, thus enhancing cell radiosensitivity.