S100A8 Promotes Chemoresistance of B-Cell Lymphoma via Autophagy
ZHOU Shixia1,2, ZHANG Li 3, LI Xiaoming1,2*, TANG Junling1,2*
BCLs (B-cell lymphomas) are malignant tumors that originate from the lymphoid hematopoietic system, resulting from the complex process of malignant transformation of lymphocytes during various stages of differentiation. The efforts to control or even eradicate BCLs are frequently hampered by the development of drug esistance. Autophagy is a regulated process of degradation and recycling of cellular constituents, which recently eceived increasing attention for its roles in conferring resistance to various commonly used anticancer therapies. S100A8 is a member of the S100 calcium-binding protein family and plays an important role in the drug resistance of lymphoid tumors, while the mechanisms are particular unclear. In the present study, by employing three BCL cell lines (Daudi, SUDHL-4 and JeKo-1), S100A8 was found to be crucial in regulating drug resistance and activating autophagy in BCL cells. Interference of S100A8 could significantly down-regulate BNIP3 expression located in mitochondrial and endoplasmic reticulum to further inhibit autophagy. In addition, S100A8 interference notably inhibited the formation of BECN1-PI3KC3 complex and promoted BCL2 expression, which collectively inhibited autophagy.
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