Ciencia y terapia del cáncer

Lenti-ShRNA-Mediated FAM54A Knockdown Suppresses Proliferation and Induces Apoptosis in Human Burkitt Lymphoma Cells

Abstract

Yang G, Wang HX, Yan B, Xu YC, Zheng YR, Chen XM, Liu FR, Zhang DZ and Jin SZ

Objectives: Burkitt lymphoma is a kind of non-Hodgkin B-cell-derived malignancy originating from germinal centre B cells. FAM54A has been proven to be involved in various physiological and pathological processes of cancers, but the biological function of FAM54A in Burkitt lymphoma remains unclear. Thus, the aim of our research was to elucidate the roles of FAM54A in the proliferation, apoptosis and cell cycle of Burkitt lymphoma.

Methods: A Burkitt lymphoma cell line (Namalwa) was chosen to perform the following experiments. FAM54AshRNA and negative control-shRNA lentiviruses that were synthesized by Qiagen were used to transfect targeted cells to knockdown FAM54A or as a negative control. Then, cell proliferation, cell cycle and cell apoptosis were detected by using MTS assay, propidium iodide staining and Annexin V-APC staining, respectively.

Results: Our results showed that high expression of FAM54A protein was found in the Namalwa cell line. Furthermore, MTS analysis revealed that knockdown of FAM54A obviously inhibited cell proliferation in Namalwa cells. Moreover, cell cycle analysis showed that knockdown of FAM54A induced Namalwa cell apoptosis and arrested the cell cycle in G2/M phase.

Conclusion: These findings suggest that FAM54A is essential for Namalwa cell proliferation and may be a potential therapeutic target for the treatment of Burkitt lymphoma.