Long intergenic non-protein coding RNA 1393 (LINC01393)

LINC01393 (long intergenic non-protein coding RNA 1393) is a cytoplasmic and nuclear long non-coding RNA that regulates gene expression via post-transcriptional and epigenetic mechanisms. In human glioblastoma, it functions as a "competing endogenous RNA" by sponging the tumor-suppressive miR-128-3p, upregulating the oncogenic protein NUSAP1, and activating the NF-κB pathway to promote cancer cell proliferation, migration, and invasion. Knockdown of LINC01393 reduces tumor growth and improves survival in animal models. In mouse embryonic stem cells, the homolog (linc1393) plays a crucial role in "pluripotency maintenance", recruiting the SET1A enzyme to induce H3K4me3 histone modification and activate pluripotency-associated genes. Expression of LINC01393 is elevated in various tumor types, suggesting broad roles in cancer biology and the potential for therapeutic targeting via RNA-based drugs[1][2].

Other names

LINC01393linc1393

Drugs (experimental): ASOs or siRNAs could block LINC01393 to reverse its transcriptional regulatory effects. Potential inhibition of LINC01393's miRNA sponge activity to restore tumor-suppressive miR-128-3p regulation and reduce oncogenic NUSAP1 levels. Interference with chromatin interaction motifs for epigenetic modulation.