LINC01559 (Long Intergenic Non-Protein Coding RNA 1559)

It also examines how the metal ions in liver cancer impact HCC growth and the efficacy of anticancer immunotherapy. Furthermore, we discuss the vital role of SLCs as key transporters for the hepatic uptake of anionic anticancer drugs, highlighting novel therapeutic opportunities.

These findings demonstrate that the acidic microenvironment influences the phenotype of DA by regulating the Linc01559-GRSF1 axis. Therefore, these findings provide potential targets for the early detection and treatment of DA.

This study identifies LINC01559 as a novel ceRNA that drives osimertinib resistance in lung adenocarcinoma by sponging miR-320a to enhance IGF2BP3 expression. Targeting the LINC01559/miR-320a/IGF2BP3 axis may provide a therapeutic strategy to overcome osimertinib resistance.

This review provides a comprehensive assessment of the clinical implications of dysregulated LINC01559 expression across various cancer types, highlighting its crucial functions and underlying molecular mechanisms in tumorigenesis. Additionally, we present in-depth discussions and propose hypotheses regarding the functional roles of LINC01559 in cancer pathogenesis, while outlining potential research avenues for future exploration of this molecular target.

LINC01559 plays an important role in LUAD metastasis through stabilizing vimentin. The expression of LINC01559 is potentially an independent prognostic factor of LUAD patients, and LINC01559 targeting may represent a novel avenue for the treatment of late-stage LUAD.

High expression levels of LINC01410 and LINC01559 were associated with low overall survival (log rank = 47.04 and 28.18, respectively, P < 0.001) and low progression-free survival (log rank = 40.68 and 28.77, respectively (P < 0.001)) and with the presence of metastasis. We suggest that LINC01559 and LINC01410 can be used as valuable, high-performing biomarkers in NSCLC diagnosis and prognosis prediction.

Our findings accentuate the salient role of FRGs as critical modulators in the pathogenesis and progression of PAAD. Importantly, our composite prognostic framework offers invaluable insights into PAAD clinical trajectory. Moreover, the complex crosstalk between FRGs and immune cell landscapes in the tumor microenvironment (TME) may elucidate prospective therapeutic strategies. The clinical translational utility of these insights, however, requires further in-depth empirical exploration. Accordingly, the FRG signature introduces a compelling new avenue for risk stratification and targeted therapeutic interventions in this devastating malignancy.

Particularly, miR-1343-3p inhibition partly abolished the suppression on docetaxel resistance in BCa cells caused by LINC01559 knockdown. To sum up, FTO-mediated epigenetic upregulation of LINC01559 promoted cell resistance to Docetaxel in BCa by negatively regulating miR-1343-3p.

Our data provide a comprehensive analysis of LINC01559 in TNBC, we found that LINC01559 functioned as a carcinogenic ceRNA via sponging miRNAs. Targeting of LINC01559 may be a potential treatment for TNBC patients.

Our study expands the repertoire of lncRNAs deregulated in PDAC, thereby revealing novel candidate biomarkers for patient risk stratification. It also provides a roadmap for functional assays aimed to characterize novel mechanisms of action of lncRNAs in pancreatic cancer, which could be explored for therapeutic development.

The results revealed a negative functional regulation of the LINC01559/miR-106b-5p/PTEN axis in CRC progression and explored a new mechanism of METTL3-mediated m6A modification on LINC01559. These results elucidate a novel potential therapeutic target for CRC treatment.

We also identified that the low expression of MEG3, LINC01963, and LINC00261 and the high expression of MACC1-AS1, LINC00462, LINC01559, and UCA1 were significantly correlated with worse survival in pancreatic cancer patients. Further research on these lncRNAs will provide new clues that could potentially improve the early diagnosis, prognostic prediction, and personalized treatments of patients with pancreatic cancer.