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ARAP1 antisense RNA 1 (ARAP1-AS1) is a **long non-coding RNA (lncRNA)** that is typically located on the antisense strand of the ARAP1 gene and does not encode protein. It is highly expressed in several types of cancer—including lung, breast, colon, and cervical cancer—where it acts as an oncogenic regulator by promoting cell proliferation, migration, and epithelial–mesenchymal transition while preventing apoptosis. Mechanistically, ARAP1-AS1 exerts its effects mainly through sponging tumor-suppressive microRNAs (such as miR-2110 and miR-4735-3p), thereby upregulating oncogenes (such as c-Myc and HDAC2), impacting cell cycle regulatory proteins like cyclin D1, and modulating key signaling pathways (including Wnt/β-catenin)[1][2][3][4][5]. Knockdown or inhibition of ARAP1-AS1 in cancer models reduces proliferation and invasiveness, suggesting its utility as a biomarker rather than a conventional therapeutic target due to its RNA nature[1][3][5].
Regulates gene expression by acting as a competing endogenous RNA (ceRNA), sponging microRNAs such as miR-4735-3p and miR-2110 to upregulate oncogenes or other effectors[1][3]. Modulates protein translation (e.g., c-Myc via interaction with PSF/PTB dimer)[1][4]. Influences cellular pathways such as the Wnt/β-catenin signaling pathway[2].
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