ELFN1 antisense RNA 1 (ELFN1-AS1)

ELFN1 antisense RNA 1 (ELFN1-AS1) is a primate-specific long non-coding RNA (lncRNA) that does not encode a protein but instead regulates the expression of other genes at the transcriptional and post-transcriptional levels[1][3]. It functions primarily through epigenetic modification, serving as a competing endogenous RNA (ceRNA) that sequesters tumor-suppressive microRNAs and as an interacting platform for chromatin-modifying proteins (such as EZH2 and DNMT3a), leading to DNA methylation and histone modification of tumor suppressor genes, thereby promoting oncogenic transcriptional programs[2][4]. ELFN1-AS1 is upregulated in several cancers, notably colorectal and gastric cancers, where it drives malignant cell proliferation, migration, immune evasion from natural killer (NK) cells, metabolic changes (such as the activation of the pentose phosphate pathway), and suppression of apoptosis. In gastric cancer, it has been shown to directly interact with TAOK1 protein kinase and inhibit the Hippo signaling pathway, resulting in increased oncogenic YAP/TAZ activity[4]. High ELFN1-AS1 expression serves as a biomarker for aggressive disease and poor prognosis, making it a putative therapeutic and diagnostic target in oncology[2][4][5]. No approved drugs currently directly target ELFN1-AS1.

Other names

MYCLo-2LOC100505644

Acts as a ceRNA/sponges tumor-suppressive microRNAs (e.g., miR-4644, miR-191-5p); Interacts with chromatin-modifying proteins (e.g., EZH2, DNMT3a) to mediate DNA methylation and histone modification at target promoters[2]; Binds protein kinases (e.g., TAOK1), influencing essential signaling pathways (e.g., inhibits Hippo signaling via suppression of STK3 phosphorylation)[4]; Promotes oncogenic transcriptional and metabolic changes (e.g., upregulation of G6PD and pentose phosphate pathway in cancer)[2]