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MELTF antisense RNA 1 (MELTF-AS1) is a long non-coding RNA (lncRNA) that is upregulated in several human cancers, including non-small cell lung cancer (NSCLC) and osteosarcoma[1][2][3]. It is located antisense to the MELTF (or MFI2) locus and can also be referred to as MFI2-AS1. MELTF-AS1 acts as an oncogenic lncRNA, promoting tumor cell proliferation, migration, invasion, and metastasis. Mechanistically, it regulates gene expression through two principal routes: - Serving as a **competing endogenous RNA (ceRNA)** that binds and inhibits specific tumor-suppressive microRNAs (e.g., miR-1299 in NSCLC and miR-485-5p in osteosarcoma), indirectly increasing pro-metastatic gene expression (such as ANXA8 and MMP14)[1][2][3]. - Interacting with the transcriptional regulator YBX1 to promote its phase separation, which activates transcription of genes involved in tumorigenesis[1]. High MELTF-AS1 expression is consistently associated with more aggressive disease, higher tumor grade and worse overall survival, suggesting both diagnostic and therapeutic potential[1][2][3]. Presently, there are no approved drugs targeting MELTF-AS1, but its modulation in preclinical studies suppresses the aggressive features of cancer cells, highlighting its promise as a target for lncRNA-based cancer therapies.
Acts as a **competing endogenous RNA (ceRNA)**, sponging microRNAs (e.g., miR-1299 in NSCLC and miR-485-5p in osteosarcoma), leading to upregulation of pro-tumorigenic genes (such as ANXA8 and MMP14) Promotes phase separation of YBX1 (a transcriptional regulator) to activate tumorigenic gene transcription
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