High expressions of BCL6 and Lewis y antigen are correlated with high tumor burden and poor prognosis in epithelial ovarian cancer

Abstract

Aberrant regulation of BCL6 plays crucial oncogenic roles in various malignant tumors; howbeit, the function of BCL6 in tumorigenesis of ovarian cancer remains unclear. The aim of this study is to investigate the role of BCL6 in ovarian cancer. The methods of immunohistochemical staining, quantitative real-time polymerase chain reaction, immunocytochemical staining, and gene expression profile enrichment analysis were performed to identify the possible role of BCL6 in ovarian cancer. We observed that the expression of BCL6 was significantly higher in ovarian cancer tissues and correlated with higher tumor burden including advanced International Federation of Gynecology and Obstetrics stages, poor differentiation, Type II ovarian cancer, the presence of >1 cm residual tumor size, and appearance of recurrence or death (all p < 0.05). The expression patterns of Lewis y were similar to these of BCL6. Multivariate Cox analysis demonstrated that advanced International Federation of Gynecology and Obstetrics stage, lymph node metastasis, residual tumor size >1 cm, as well as high expressions of BCL6 and Lewis y antigen were independent factors of worse progression-free survival and overall survival (all p < 0.05). There was a positive correlation of the expressions of BCL6 and Lewis y antigen. The associated genes with BCL6 in response to Lewis y antigen were identified, including four upregulated genes ( SOCS3, STAT1, PPARG, and GADD45A) and three downregulated genes ( ACAN, E2F3, and ZBTB7B). In conclusion, the high expressions of BCL6 and Lewis y antigen are associated with development, high tumor burden, and worse prognosis of ovarian cancer and targeting BCL6 could be a novel therapeutic strategy for ovarian cancer treatment.

miR-144-3p inhibits cell proliferation of colorectal cancer cells by targeting BCL6 via inhibition of Wnt/β-catenin signaling

“…B-cell lymphoma 6 (BCL6), also known as BCL6A, LAZ3, or ZNF51, belonging to the BTB-POZ protein family, has been demonstrated to facilitate cell proliferation [17]. Reports showed that BCL6 may be a novel diagnostic and treatment strategy for breast or ovarian cancer [27,28]. However, the role BCL6 plays in CRC remained unknown.…”

miR‑339‑5p inhibits lung adenocarcinoma invasion and migration by directly targeting BCL6

“…For instance, BCL6 promoted glioma and served as a therapeutic target ( 26 ). high Lewis y antigen and BCL6 expressions in epithelial ovarian cancer were associated with poor prognosis and high tumor burden ( 27 ). BCL6 was increased and downregulated by miR-544 in triple-negative breast cancer to suppress tumor growth ( 28 ).…”

LINC00152 Promotes Tumor Progression and Predicts Poor Prognosis by Stabilizing BCL6 From Degradation in the Epithelial Ovarian Cancer

“…Since lncRNAs could either repress (20) or prompt (21) the ubiquitination of target substrates, it is unclear whether the molecular mechanisms of LINC00152 in EOC are linked to the ubiquitination of downstream proteins. B-cell CLL/lymphoma 6 (BCL6) is a highly conserved zinc finger transcriptional factor and is implicated in the pathogenesis of human B-cell lymphomas by controlling the transcription of oncogenes (22). Previous studies demonstrate that BCL6 is degraded via the ubiquitin-proteosome system (23,24) and its degradation is balanced by FBXO11 (23) and AIP (25) thus regulating the tumor growth of diffuse large B cell lymphoma.…”

“…Previous studies demonstrate that BCL6 is degraded via the ubiquitin-proteosome system (23,24) and its degradation is balanced by FBXO11 (23) and AIP (25) thus regulating the tumor growth of diffuse large B cell lymphoma. Recently BCL6 has also been reported to be dysregulated in somatic malignancies such as breast carcinoma (26,27) and EOC (22,28). However, it remains unclear whether degradation of BCL6 is related to lncRNAs and how the interaction is implicated in the tumorigenesis of somatic malignancies.…”