APCDD1L-DT (APCDD1L Divergent Transcript)

The tumor-infiltrating immune cells, chemotherapeutics efficacy, and expression of immune checkpoint genes were also evaluated between the high- and low-risk groups. The prognostic signature consisting of irlncRNAs could predict the prognosis and immune landscape of patients with ICC and may provide a novel perspective for the individualized intervention in ICC.

Overall, our data confirm that APCDD1L-AS1 is upregulated by hypoxia-induced HIF-1α, which drives the TCA cycle by stabilising DLST to further promote osimertinib resistance in LUAD. Our findings provide new insights into the role of HIF-1α/APCDD1L-AS1/DLST axis-related reprogramming of hypoxia and the TCA balance in conferring osimertinib resistance in LUAD and confirm the therapeutic potential for targeting the APCDD1L-AS1.

Furthermore, the lncRNAs of the signature were prioritized, with the top five being TMEM105, DUXAP8, APCDD1L-DT, PCAT6, and a novel transcript, ENSG00000226308. Furthermore, both Kyoto Encyclopedia of Genes and Genomes pathway and Disease Ontology analyses provided strong support for the viability of this model-independent signature, emphasising ENSG00000226308 as a promising biomarker.

This activation, in turn, propels the abnormal activation of the Wnt pathway, fostering tumor development by impeding the ubiquitin-mediated degradation of DVL2. Broadly speaking, this study provides auspicious perspectives for comprehending CCA and furnishes support for addressing this daunting malignancy.

Our study established a concise CDG-RlncRNA signature and underscored the pivotal role of SNHG3 in ccRCC progression. It emphasizes the clinical relevance of CDG-RlncRNAs in prognostic prediction and targeted therapy, offering potential avenues for personalized intervention in ccRCC.

This 8-CRlncRNAs risk model may be promising for the clinical prediction of prognoses, tumor immune, immunotherapy response and chemotherapeutic response in KIRC patients.

The developed risk signature takes on critical significance in the prediction of the prognosis of patients with KIRC, and it can bring a novel direction for immunotherapy and clinical drug treatment of KIRC. In addition, 4 identified risk LncRNAs (especially APCDD1L-DT and MINCR) can be novel targets for immunotherapy of KIRC patients.

APCDD1L-AS1 was able to inhibit the progression of ccRCC, and its decreased expression could be caused by DNA hypermethylation and loss of VHL protein expression. Therefore, APCDD1L-AS1 may serve as a new therapeutic target in the treatment of ccRCC.

Further, extensive immune cells were upregulated in the high-risk group, such as CD8 T cell, neutrophil, macrophage, and myeloid dendritic cell, indicating increased immune infiltrations. We established a novel ferroptosis-related lncRNA signature that could effectively stratify the prognosis of glioma patients with adequate predictive performance.

Moreover, NSD2 upregulation neutralized the influence of blocking APCDD1L-AS1 in HSC-3/5-FU and HN-4/5-FU cells on 5-FU resistance. To sum up, our study demonstrated that exosomal APCDD1L-AS1 conferred resistance to 5-FU in HSC-3/5-FU and HN-4/5-FU cells via the miR-1224-5p/NSD2 axis, thus providing a novel target for OSCC chemoresistance.