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THAP7 antisense RNA 1 (THAP7-AS1) is a long non-coding RNA (lncRNA) transcribed antisense to the THAP7 gene. It is not translated into a protein but exerts functional roles through its RNA structure and interactions. THAP7-AS1 is transcriptionally activated by the transcription factor SP1 and its stability is enhanced by m^6A modification via METTL3, with dependence on the RNA-binding protein IGF2BP1. In gastric cancer, THAP7-AS1 is significantly upregulated and acts as an oncogenic lncRNA. It promotes tumor cell growth, migration, and invasion both in vitro and in vivo by interacting with CUL4B (an E3 ubiquitin ligase) and importin α1, aiding CUL4B nuclear localization. Through this pathway, it represses tumor- suppressive microRNAs (miR-22-3p and miR-320a) via chromatin modifications, thereby activating the PI3K/AKT oncogenic pathway and contributing to cancer progression. High THAP7-AS1 expression is associated with lymph node metastasis and poor prognosis, and silencing it suppresses tumor growth, making it a promising potential molecular target in gastric cancer therapies[1][2][4]. No evidence exists that THAP7-AS1 codes for a protein or acts as a classical receptor, enzyme, transporter, or ion channel. It functions instead as an oncogenic regulator at the RNA level.
Therapeutic approaches include knockdown or silencing of THAP7-AS1 (e.g., shRNA, antisense oligos) to suppress gastric cancer growth, invasion, and metastasis[1]
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