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Leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1) is a long non-coding RNA (lncRNA) transcribed antisense to the LIFR gene on human chromosome 5p13.1[6]. LIFR-AS1 has been found to regulate diverse biological processes at the transcriptional and post-transcriptional level, including proliferation, migration, invasion, apoptosis, and drug resistance in multiple cancer types[1][6]. Mechanistically, LIFR-AS1 functions primarily as a molecular sponge for various microRNAs, influencing oncogenic or tumor-suppressive pathways such as MAPK, NF-κB, and MEK/ERK[1][6]. Its expression is deregulated in many cancers; in some contexts, LIFR-AS1 acts as a tumor suppressor, while in others it exhibits oncogenic activity. Altered levels of LIFR-AS1 are associated with cancer prognosis, clinicopathological features, and chemotherapeutic response, suggesting it may serve as both a biomarker and potential therapeutic target in oncology[6][1][5]. Key points: - Not a receptor or enzyme, but an antisense lncRNA. - Emerging as a functional biomarker and regulative target in cancer, mostly via RNA-based mechanisms[6][1]. - No known direct pharmacological drugs, but indirect modulation of drug resistance has been reported (e.g., temozolomide in glioma)[6].
Modulation of microRNA sponging (e.g., miR-4262, miR-197-3p, miR-29a-3p, miR-31-5p), Regulation of signaling pathways (NF-κB, MEK/ERK, MAPK), Indirectly alters pathway activity and gene expression related to tumor suppression or progression[6][1]
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