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YW
Verified CAS / Academic Author2 Decoded Studies

Prof. YU Wenfeng

Guizhou Medical University

Research Publications & English Decoded Briefs

Showing 2 publications
Acta Biochimica et Biophysica Sinica2025DOI: 10.3724/abbs.2025032

Long noncoding RNA UCA1 knockdown inhibits cisplatin-resistant cervical cancer tumorigenesis via the miR-195-5p/IKBKB axis

Cisplatin resistance is a major cause of poor prognosis in patients with cervical cancer. Dysregulation of long noncoding RNAs (lncRNAs) plays a key role in chemoresistance. Our results reveal that the lncRNA UCA1 is upregulated in cisplatin (DDP)-resistant cervical cancer tissues and HeLa cells. Mechanistically, the lncRNA UCA1 acts as a sponge for miR-195-5p, targeting IKBKB. UCA1 enhances proliferation, migration, and invasion while reducing apoptosis in DDP-resistant HeLa cells via the miR-195-5p/IKBKB axis. Additionally, UCA1 upregulates BNIP3Δex2 and p-p65 expressions and downregulates BNIP3 expression in DDP-resistant HeLa cells. Abnormal expressions of BNIP3Δex2 and BNIP3 significantly alter the malignant progression of HeLa/DPP cells. In vivo, UCA1 silencing inhibits growth, enhances apoptosis, and upregulates IKBKB, BNIP3Δex2, and p-p65 expressions while downregulating BNIP3 expression in subcutaneous xenografts in nude mice by targeting miR-195-5p. Overall, this study highlights a novel promising target for the treatment of DDP-resistant cervical cancer.

Acta Biochimica et Biophysica Sinica2025DOI: 10.3724/abbs.2025032

Long noncoding RNA UCA1 knockdown inhibits cisplatin-resistant cervical cancer tumorigenesis via the miR-195-5p/IKBKB axis

Cisplatin (DDP) resistance remains a principal determinant of poor prognosis in cervical cancer, with five-year survival at 16.5% for recurrent or advanced metastatic disease. The long noncoding RNA UCA1 is upregulated in DDP-resistant cervical cancer tissues and HeLa cells. Mechanistically, UCA1 functions as a competing endogenous RNA for miR-195-5p, thereby derepressing IKBKB. UCA1 knockdown suppresses proliferation, migration, and invasion while increasing apoptosis in DDP-resistant HeLa cells through the miR-195-5p/IKBKB axis. UCA1 upregulates BNIP3Δex2 and p-p65 and downregulates BNIP3 in DDP-resistant HeLa cells; forced changes in BNIP3Δex2 and BNIP3 expression significantly alter malignant progression of HeLa/DDP cells. In subcutaneous xenografts in nude mice, UCA1 silencing inhibits tumor growth, enhances apoptosis, and upregulates IKBKB, BNIP3Δex2, and p-p65 while downregulating BNIP3 via miR-195-5p targeting. These findings identify UCA1 as a promising therapeutic target for DDP-resistant cervical cancer.