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Apoptosis-associated transcript in bladder cancer (AATBC) is a long intergenic noncoding RNA (lincRNA) identified as being highly expressed in bladder cancer tissues and cell lines, with expression positively correlating with tumor grade and stage. Functionally, AATBC acts as an oncogenic lncRNA, promoting cell proliferation and inhibiting apoptosis by modulating cell cycle proteins (cyclin D1, CDK4, p18, phosphorylated Rb) and regulating intrinsic apoptotic pathways (caspase-9, caspase-3). Knockdown of AATBC activates the JNK signaling pathway and suppresses NRF2, resulting in increased apoptosis. Inhibition of AATBC has been shown to suppress tumor growth both in vitro and in vivo, supporting its potential as a therapeutic target and biomarker in bladder cancer. There are no current approved drugs directly targeting AATBC; however, its inhibition synergizes with cisplatin, and JNK inhibitors can modulate apoptosis induced by AATBC knockdown. AATBC is encoded by a transcript located on human chromosome 21q22.3 with a length of 4,622bp and is classified as a non-protein-coding gene. No evidence currently supports its involvement beyond bladder cancer or as a receptor, enzyme, transporter, or classical drug target family; it is a regulatory RNA molecule.
Knockdown of AATBC (using siRNAs) induces cell cycle arrest (G1 phase), promotes apoptosis via activation of intrinsic pathway (caspase-9, caspase-3), and is synergistic with cisplatin, suggesting AATBC's role in chemoresistance. SP600125 blocks JNK activation, reducing apoptosis induced by AATBC inhibition.
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