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Gastric cancer associated transcript 3 (GACAT3) is a long non-coding RNA (lncRNA) located on human chromosome 2p24.3[2][1][3]. It does not encode a protein but acts as a regulatory RNA, prominently functioning as a competing endogenous RNA (ceRNA) that sponges specific microRNAs. GACAT3 is upregulated in various malignancies, including gastric, colorectal, hepatocellular, breast, bladder, ovarian, lung cancer, and glioma, and promotes oncogenic properties such as cell proliferation, migration, invasion, and epithelial-mesenchymal transition, while inhibiting apoptosis[2][1]. Its expression correlates with disease stage, tumor size, and poor clinical outcomes, making it a promising biomarker for cancer diagnosis, prognosis, and potentially as a therapeutic target[2]. GACAT3’s principal mechanism involves modulating the activity of oncogenic or tumor-suppressive microRNAs, with downstream effects on proteins like p21, BAX, E-cadherin, Ki-67, STAT3, and others relevant to tumor progression[2][1]. There are currently no approved drugs directly targeting GACAT3, but its role in cancer signaling suggests interest in its modulation for future therapeutic strategies.
Not drug-targeted; molecular mechanisms include acting as a competing endogenous RNA (ceRNA) for various microRNAs (e.g., miR-129-5p, miR-497, miR-103, miR-135a, miR-3127-5p), regulation of key cancer-related pathways (such as IL6/STAT3), sponging microRNAs to regulate cancer cell proliferation and migration
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