Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway

Abstract EN

Background.

BCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers.

This study was to detect the expression of BCL6 and its biological effect on glioma.

Methods.

RT-PCR and Western blot were used to detect the expression of BCL6 mRNA and protein in tissues and glioblastoma cell lines.

The expression of BCL6 was knockdown in two glioblastoma cell lines (U87 and U251) using BCL6 shRNA.

The CCK8, colony-formation, flow cytometry, Transwell, and wound-healing assays were used to evaluate the malignant phenotypic change of glioblastoma cells.

Results.

The expression of BCL6 was higher in glioma tissues and glioblastoma cell lines than normal tissues.

Knockdown of BCL6 expression reduced the proliferation, migration, and invasion of glioblastoma cells.

Moreover, knockdown of BCL6 changed expression of proteins related to malignant behaviors of glioblastoma cells.

The suppression of BCL6 could increase chemosensitivity of U87 and U251 to temozolomide.

Downregulation of BCL6 levels suppressed the expression of BCL2, cyclin D1, MMP2, and MMP9 proteins as well as two classic signaling pathway proteins p-AKT and p-ERK.

Simultaneously, BAX and p21 protein levels were upregulated along with knockdown of BCL6.

Conclusions.

Our results indicated that BCL6 may be a tumor oncogene involved in the progression of glioma via affecting AKT and MAPK signaling pathways.