LINC00461 (Long Intergenic Non-Protein Coding RNA 461)

Furthermore, the study identified a significant enrichment of microRNA target genes within the samples examined, suggesting a potential regulatory relationship between these molecules and their target genes. Consequently, this investigation has constructed competing endogenous RNA networks and has further elucidated the underlying biomarkers for breast cancer cohorts.

In this study, we report lncRNAs (PVT1, FAM13A-AS1, LINC00461, NAV2-AS5, PRICKLE2-AS1, and VCAN-AS1) that may function as oncogenes or tumor suppressors by regulating the expression of coding genes, such as RAB24, HECW2, LGR4, and FKBP5. These lncRNAs and coding genes may play important roles in LUSC development and progression.

Moreover, we found that LINC00461 regulated HNRNPUL1 expression through miR-518b sponge activity, and the miR-518 inhibitor could reverse the inhibitory effects of LINC00461 knockdown on BC cell proliferation, migration, and EMT. Our results suggest that LINC00461 may serve as a potential biomarker and therapeutic target for BC.

Intriguingly, increased expression of lncRNA ST20 coupled with RAG1 demonstrated a favorable prognostic impact on OS, EFS, and RFS. Conclusively, several hitherto unreported associations of gene expression patterns with clinicopathologic features and prognosis were identified, which may help understand T-ALL's molecular pathogenesis and provide prognostic markers.

Collectively, homolog clustering via the highly conserved region definition and detection on long non-coding RNAs, as well as the functional explorations on representative sequences in our research, would provide new evidence for the potential function of long non-coding RNAs. Our results on the remarkable roles of long non-coding RNAs would presumably provide a new theoretical basis and candidate diagnostic indicators for tumors.

Knockdown of LINC00461 enhanced the therapeutic effects of ixazomib against multiple myeloma in part by the regulation of SNRPB2.

The inhibition of LINC00461 or overexpression of miR-411-5p reduced the expression of BNIP3 protein, thereby inducing apoptosis at the in vivo and in vitro levels. LINC00461 may induce miR-411-5p to "sponge," thereby increasing the expression of BNIP3 protein, and exerting the function of inhibiting apoptosis and promoting DLBCL recurrence.

LINC00461 is involved in resistance to four anticancer drugs, including sunitinib for renal cell carcinoma, cisplatin for head and neck squamous cell carcinoma and rectal cancer, temozolomide for glioma, and docetaxel for breast cancer. Notably, knockdown of LINC00461 in exosomes antagonizes tumor cell proliferation in multiple myeloma. This article summarizes the diagnostic, prognostic, and therapeutic value of LINC00461 in various tumors, and systematically describes the ceRNA network and signaling pathways associated with LINC00461, providing potential directions for future LINC00461 research.