Y. M. Viletska*, M. Y. Sliusar, A. I. Abramchuk, O. V. Halkin,
O. O. Ratushna, O. Y. Luzina, O. H. Minchenko

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
*e-mail: yulya.viletska@ukr.net

Received: 19 September 2025; Revised: 13 October 2025;
Accepted: 03 April 2026; Available on-line: April 2026

Endoplasmic reticulum (ER) stress and hypoxia interaction in the progression of glioblastomas and other malignant tumors has not yet been sufficiently studied. Both PSAT1, as the ER stress-responsive phosphoserine aminotransferase, and сyclin D1 are shown to participate in tumor progression and chemoresistance. Therefore, this study aimed to elucidate the effect of endoplasmic reticulum stress on PSAT1 and CCND1 (сyclin D1) genes expression in normal human astrocytes of NHA/TS line, and U87MG glioblastoma cells. Hypoxia was created with the HIF1A prolyl hydroxylase inhibitor dimethyloxalylglycine. Tunicamycin and thapsigargin were used for ER stress induction. PSAT1 and cyclin D1 expression were examined by quantitative real-time RT-PCR. It has been established that hypoxia and tunicamycin had a similar suppressive effect on PSAT1 and CCND1 expression in normal astrocytes, but increased both genes expression in glioblastoma cells. Thapsigargin enhanced PSAT1 expression in both cell lines, but suppressed CCND1 expression in normal astrocytes without any effect on its expression in glioblastoma cells. Hypoxia modified the effect of tunicamycin and thapsigargin when these ER stress inducers were combined with hypoxia, but in different ways in normal and glioblastoma cells. These results indicate that hypoxia and ER stress relationship in the control of the studied genes expression differs in normal and tumor cells.