Long non-coding RNA urothelial carcinoma-associated 1 (UCA1)

Long non-coding RNA urothelial carcinoma-associated 1 (UCA1) is a non-protein coding transcript initially identified in bladder cancer but now recognized as an oncogenic lncRNA overexpressed in numerous human cancers[1][2][3]. UCA1 promotes tumor progression by enhancing cell proliferation, migration, and survival through its function as a competitive endogenous RNA, sponging tumor-suppressive microRNAs and deregulating key signaling proteins involved in cancer pathogenesis (including Wnt/β-catenin, AKT/mTOR, CREB1, and PDL1)[1][2][3]. UCA1 has been strongly implicated in mediating resistance to various anti-cancer drugs such as cisplatin, tamoxifen, and 5-fluorouracil, and is considered both a mechanistic contributor to multidrug resistance and a promising diagnostic, prognostic, and therapeutic biomarker in oncology[1][2][3]. Studies suggest it is a candidate therapeutic target for reversing drug resistance or improving immune-based therapies in multiple malignancies[1][2].

Other names

UCA1 antisense RNA 1UCA1-AS1CLEC4OLINC01835C-type lectin domain family 4 member Olong intergenic non-protein coding RNA 1835CLEC4OP

Acts as a competing endogenous RNA (ceRNA) that sponges multiple microRNAs (e.g., miR-26a, miR-26b, miR-193a, miR-204, miR-214, miR-18a), resulting in upregulation of oncogenes and drug resistance genes[1][2][3] - Promotes activation of signaling pathways such as Wnt/β-catenin, AKT/mTOR, and CREB1 leading to proliferation, inhibition of apoptosis, immune escape, and drug resistance[1][2][3]