BCL9 enhances the development of cervical carcinoma by deactivating CPEB3/EGFR axis

Purpose: To investigate the differential expression of BCL9 in cervical carcinoma samples, analyze its biological functions in regulating malignant phenotypes of cervical carcinoma cells, and to explore its potential molecular mechanism. Methods: Expression levels of BCL9 in 58 pairs of cervical carcinoma tissues and paracancerous tissues were determined using quantitative real time-polymerase chain reaction (qRT-PCR). Kaplan Meier curves were used to analyze the prognostic potential of BCL9 in cervical carcinoma. After knockdown using BCL9 by lentivirus transfection, proliferative and migratory changes in Siha and HeLa cells were determined by CCK-8, colony formation and Transwell assays. Cytoplasmic polyadenylation element binding protein 3 (CPEB3), the potential downstream target of BCL9, was confirmed via dualluciferase reporter assay. Western blot analyses were conducted to determine the protein levels of CPEB3, EGFR, AKT and p21 in Siha and HeLa cells with BCL9 knockdown. The co-regulation of BCL9 and CPEB3 on phenotypes of cervical carcinoma cell was investigated. Results: BCL9 was upregulated in cervical carcinoma tissues. The high level of BCL9 was predicted by the tumor size, advanced stage and poor prognosis. The knockdown of BCL9 significantly weakened proliferative and migratory abilities of Siha and HeLa cells (p < 0.05). CPEB3 was the downstream target of BCL9, and was lowly expressed in cervical carcinoma tissues. The knockdown of BCL9 upregulated CPEB3, and downregulated EGFR, AKT and p21 (p < 0.05). The knockdown of CPEB3 also reversed the influence of silenced BCL9 in regulating its proliferative and migratory abilities in cervical carcinoma cells (p < 0.05). Conclusion: BCL9 drives the deterioration of cervical carcinoma by inhibiting the CPEB3/EGFR axis. Thus, BCL9 may be a novel molecular target for cervical carcinoma treatment.