O. V. Halkin*, Y. M. Viletska, M. Y. Sliusar, S. V. Danilovskyi,
Y. V. Kulish, O. V. Rudnytska, O. H. Minchenko

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
*e-mail: oleggal2014@gmail.com

Received: 07 October 2025; Revised: 10 December 2025;
Accepted: 30 January 2026; Available on-line: February 2026

Hypoxia and ER stress are obligate factors in tumor growth, however, the interaction between these factors has not been sufficiently studied. Heat shock proteins HSPA5 and DNAJB9 as a key components of the endoplasmic reticulum stress response play an important role in the growth of malignant tumors, including glioblastomas. This study aimed to investigate the interaction between hypoxia and ER stress in controlling HSPA5 and DNAJB9 expression in glioblastoma cells and normal astrocytes. Hypoxia was created with dimethyloxalylglycine, ER stress was induced with tunicamycin and thapsigargin, HSPA5 and DNAJB9 expression was studied by qPCR. It has been established that in astrocytes HSPA5 and DNAJB9 expression was resistant to hypoxia. However, in glioblastoma cells, the expression of these genes under hypoxia was increased. Tunicamycin and thapsigargin enhanced HSPA5 and DNAJB9 expression with a much stronger effect in glioblastoma cells. When these ER stress inducers were combined with hypoxia their effect was modified to a greater extent in normal astrocytes. The obtained results indicate different cell-specific sensitivity of HSPA5 and DNAJB9 expression to hypoxia and ER stress inducers.

Keywords: DNAJB9, endoplasmic reticulum stress, gene expression, glioblastoma cells, HSPA5, hypoxia, normal human astrocytes