Up-regulation of
heat shock protein 70 (HSP70) could be elicited primarily by heat in former studies, and this was proved to be associated with
cancer progression.
Burkitt's lymphoma is one of highly aggressive B-cell
non-Hodgkin's lymphoma and is one of the fastest growing human
tumors. To investigate the effect of HSP70 expression on the sensitivity of human
Burkitt lymphoma cells (Raji cells) to
chemotherapy and its role in the involvement of PI3K/AKT pathway, we evaluated the effects of
LY294002, a PI3K inhibitor, on the expression of HSP70 and cell sensitivity to
adriamycin (ADM) or
cisplatin (DDP). In present study, expressions of HSP70, AKT and phosphorylated AKT (p-AKT) in Raji cells were measured by Western-Blot. Apoptosis index of Raji cells was examined by flow cytometry. Cytotoxicities of
adriamycin (ADM) and
cisplatin (DDP) were determined by
WST-8 assay. We found that
hyperthermia (42 degrees for 1 hour) up-regulated the expression of HSP70 expression and blockade of PI3K/AKT pathway down-regulated HSP70 expression in Raji cells. Compared to cells treated with ADM or DDP alone,
hyperthermia protected cells from
chemotherapy while
LY294002 enhanced sensitivity of Raji cells to
chemotherapy. Our results suggested down-regulation of HSP70 expression by blockade of PI3K/AKT pathway maybe responsible for the increased sensitivity of Raji cells to
chemotherapy. Targeting PI3K/AKT pathway or inhibiting HSP70 expression may be beneficial for
chemotherapy treatment of
Burkitt lymphoma patients.