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MCF2L antisense RNA 1 (MCF2L-AS1) is a long non-coding RNA located on chromosome 13, opposite to the MCF2L gene[1]. It does not encode a protein but exerts its biological effects through RNA-mediated regulation of gene expression. MCF2L-AS1 has been established as an oncogenic lncRNA that is overexpressed in multiple cancers (including breast, colorectal, lung, ovarian, and liver cancer). Experimental studies have shown that increased MCF2L-AS1 expression contributes to tumor cell proliferation, migration, invasion, and resistance to chemotherapeutic agents. Mechanistically, it interacts with several microRNAs (such as miR-33a-5p, miR-105-5p, miR-874-3p, and miR-873-5p), and upregulates oncogenic factors including FGF2, RAB22A, and FOXM1, often through acting as a competing endogenous RNA. In breast cancer, MCF2L-AS1 directly binds to the transcriptional co-activator YAP, facilitating malignant behavior through Hippo pathway modulation[4]. Its expression correlates with poor prognosis and increased metastatic potential, suggesting value as both a biomarker and a potential therapeutic target in oncology[2][3][4]. There are currently no drugs directly targeting MCF2L-AS1 in clinical use, but modulation of its expression alters tumor biology and drug responsiveness in preclinical studies.
Regulates tumor progression and metastasis by binding to and activating Yes-associated protein (YAP) (a key regulator in the Hippo signaling pathway); modulates gene expression via competitive endogenous RNA mechanisms (ceRNA) including sponging miR-33a-5p, miR-105-5p, miR-873-5p, and upregulating FGF2, RAB22A, FOXM1, IL-1β
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