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MYOSLID antisense RNA 1 (MYOSLID-AS1), often referred to as MYOSLID, is a cytoplasmic long non-coding RNA classified as a natural antisense transcript. It was first identified as a serum response factor (SRF)-dependent lncRNA that amplifies the vascular smooth muscle cell (VSMC) differentiation program by promoting F-actin assembly and enabling the nuclear translocation of MKL1, which in turn activates VSMC contractile genes[1]. MYOSLID is transcriptionally regulated by MYOCD and SRF, and its expression is closely tied to VSMC biology and vascular remodeling processes[1]. More recently, MYOSLID has been implicated in oncogenesis, where it functions as a competing endogenous RNA (ceRNA), sponging tumor-suppressive microRNAs (e.g., miR-29c-3p) to elevate oncogene expression and promote cancer cell proliferation, migration, and resistance to cell death[3][4]. Its expression is upregulated in various human cancers, including colorectal and gastric cancers, and correlates with poor prognosis and altered tumor immune landscapes[4]. While MYOSLID is studied as a molecular and prognostic biomarker, it is not currently recognized as a therapeutic target in the sense of a druggable receptor, enzyme, or transporter. The entry "MYOSLID antisense RNA 1" likely conflates the original lncRNA (MYOSLID) with a more formalized NAT designation, but MYOSLID-AS1 is not widely used as a canonical name; the established name in the literature is "MYOSLID" or "MYOSLID lncRNA" referring to the same entity[1][3][4].
Acts as a molecular sponge for microRNAs (e.g., miR-29c-3p), thereby affecting the expression of oncogenes such as MCL-1 in gastric cancer[3]
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