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TGF-beta induced TARBP2 interacting long non-coding RNA (TGILR) is a long non-coding RNA (lncRNA) located at chromosome 6p25.2 that is transcriptionally activated by the canonical TGF-beta/SMAD3 signaling pathway, particularly in cancer. TGILR directly interacts with the RNA-binding protein TARBP2, destabilizing it and consequently perturbing microRNA biogenesis—specifically reducing levels of tumor-suppressive miR-1306 and miR-33a. This promotes the activation of EMT-related transcriptional programs (notably via TCF4), thereby enhancing gastric cancer cell proliferation, invasion, and metastasis. High TGILR expression is closely associated with poor prognosis and lymph node metastasis in gastric cancer, and constitutes a potential prognostic biomarker and putative therapeutic target in the tumor microenvironment, specifically where TGF-beta signaling is overactivated due to cancer-associated fibroblast infiltration[1][5].
Not applicable; as an lncRNA, TGILR is not (as yet) the direct molecular target of existing approved drugs. Research focuses on its knockdown or the inhibition of its upstream pathway (e.g., TGF-beta or CAF-targeted therapies)[1].
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