Hyperthermia enhances bortezomib-induced apoptosis in human white blood cancer cells

Dinara Baiskhanova, Timur Saliev, Dinara Begimbetova, Loreto B. Feril, Anton Klodzinskyi, Katsuro Tachibana, Xeniya Merinyanu

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


At present, the current therapeutic strategy for apoptosis induction mainly relies on the administration of
pharmacological apoptotic modulators. Apart from that, apoptosis can be induced by various external stimuli
such as hyperthermia, ionizing radiation, and electric fields. Despite advantages, both physical and pharmacological
approaches bear some limitations as well. The rationale of this study was to overcome the limitations
by combining hyperthermia and apoptotic modulator ‘bortezomib’ (Velcade). Two types of human blood cancer
cell lines were utilized: human leukemic monocyte lymphoma cell U937 line and peripheral blood mononuclear
cells (PMBCs) derived from the patient diagnosed with acute myeloid leukemia. Prior to apoptosis experiments,
cytotoxicity tests were performed at three types of temperature regimes (40 °, 42 ° and 44 °C). We observed a
gradual inhibition of cell viability correlating with an increase of temperature and drug concentration in both
cell lines. However, there was no significant difference between sham group and groups of leukemic PMBCs
treated by high temperature (44 °C) and bortezomib. In U937 cells, combined treatment by heat shock and
bortezomib led to an increase the number of cells underwent the late apoptosis stage. At the same time, similar
treatment of PMBCs resulted in the stimulation of early apoptosis. Our data suggest that combination of
bortezomib and hyperthermia enhances apoptosis induction in human cancer white blood cells, indicating a
therapeutic potential for blood cancer therapy.
Original languageEnglish
Pages (from-to)9-14
Number of pages6
JournalJournal of Thermal Biology
Publication statusPublished - 2017


  • Hyperthermia, cytotoxicity, apoptosis, bortezomib, velcade, blood cancer

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