Lnc00892 enhances cisplatin sensitivity by inducing apoptosis through the BTAF1/MDM2/STAT5B/XIAP axis in bladder cancer cells

BACKGROUND: Chemotherapy is the primary mode of treatment for patients with advanced bladder cancer. However, because of their non-specificity, chemotherapy drugs induce many notable side effects in patients. Recent studies have shown that the expression of certain long non-coding RNAs (lncRNAs) is closely related to the sensitivity of tumors to chemotherapeutic drugs. Thus, lncRNAs can be exploited as markers of tumor chemotherapeutic sensitivity to improve the efficacy of chemotherapy. Here, we investigated the role of the lnc00892 in the response of bladder cancer cells to cisplatin. RESULTS: Mechanistically, both RNA pull down assay and RIP experiment showed lnc00892 bound to BTAF1, which accelerated the dissociation of TFIID from the MDM2 promoter region in cisplatin-treated bladder cancer cells. This process reduced the transcription of MDM2, promoting STAT5B protein degradation through the ubiquitination-mediated pathway. Ultimately, these events attenuated XIAP transcription and promoted bladder cancer cell apoptosis. CONCLUSION: Lnc00892 promoted bladder cancer cells apoptosis by binding to BTAF1 which further reduced MDM2/STAT5B/XIAP levels, and ultimately promoted the sensitivity of bladder cancer cells to cisplatin. Lnc00892 could be used as a marker of cisplatin chemosensitivity in the clinic to improve the outcomes of patients with bladder cancer.