LINC01116 (Long Intergenic Non-Protein Coding RNA 1116)

Our findings unveil a novel LINC01116/miR-432-5p/FKBP7/14 axis that drives melanoma stemness and protein synthesis addiction. These insights identify promising therapeutic targets for melanoma intervention.

Efficient knockdown of LINC01116 in LEC in normoxic or hypoxic conditions impacted the proliferation rate under hypoxic stimulation and revealed a gene signature associated with proliferation and hypoxia sensing. Together, our data suggest a role for LINC01116 in pathological lymphangiogenesis of lung tumors.

Among these, we further validated LINC00704 and LINC01116 as proliferation-regulating lncRNAs in cSCC lines and potential biomarkers of cSCC growth. Taken together, our study provides a comprehensive signature of lncRNAs with roles in regulating cSCC growth.

The study presents a novel prognostic model based on 14 autophagy-related LncRNAs for patients with lung adenocarcinoma. This model may further guide the clinical treatment of lung adenocarcinoma.

MAT suppresses BC cell and EMT proliferation via the LINC01116/miR-9-5p/ITGB1 pathway. Thus, MAT may be a promising target for adjuvant anti-BC therapy.

linc01116 is upregulated in most cancers, and this upregulation is associated with a poor prognosis. Therefore, linc01116 serves as a promising therapeutic target and prognostic biomarker for cancer.

The downregulation of miR-9-5p significantly reduces the CCNE1 level in A549 cells, and the upregulation of LINC01116 counteracts the downregulation of miR-9-5p effect, restoring the expression level of CCNE1. Our data demonstrated that LINC01116 regulates the expression of CCNE1 by positively regulating miR-9-5p, thereby affecting cell cycle, proliferation and participating in the development of LUAD.

Hence, LINC01116 may serve as a prognostic biomarker and therapeutic target for human cancer. This paper summarizes the current evidence regarding the biological functions and molecular mechanisms of LINC01116 in the progression of cancer, providing theoretical references for LINC01116-related cancer treatment in the future.

Twelve differential m6A regulators were identified, and RBM15 was found to be correlated positively with the hub lncRNA AL606489.1. Our study constructed a prognostic risk model based on anoikis-related lncRNAs, which could provide novel perspective on the prognosis of LUAD patients.

Among these, we further validated LINC00704 and LINC01116 as proliferation-regulating lncRNAs in cSCC lines and potential biomarkers of cSCC progression. Taken together, our study provides a comprehensive signature of lncRNAs with roles in regulating cSCC progression.

Subsequent transformation activates multiple oncogenes (e.g., EGFR, miR-21, and WEE1), driven by the SOX2- and OLIG2-dependent glioma-specific super enhancers. These results help reconstruct the sequence of events underlying the process of astrocyte transformation, highlighting HOXDeRNA's central genome-wide activity and suggesting a shared RNA-dependent mechanism in otherwise heterogeneous and multifactorial gliomagenesis.

Collectively, our findings reveal, for the first time, that LINC01116 enhances Pol I transcription by scaffolding essential transcription factors to the ribosomal DNA promoter, thereby driving oncogenic activities in LUAD. We propose the c-Myc-LINC01116-Pol I axis as a critical oncogenic pathway and a potential therapeutic target for modulating Pol I transcription in LUAD.