TY - JOUR

T1 - Фактор роста нервов: влияние на миграцию, клоногенность и биоэнергетический метаболизм митохондрий клеток глиомы U251

AU - Chernov, A.N.

AU - Glushakov, R.I.

AU - Landynya, S.S.

AU - Sharapov, Y.A.

AU - Galimova, E.S.

AU - Shamova, O.V.

N1 - Export Date: 01 November 2025; Cited By: 0; Correspondence Address: A.N. Chernov; Institute of Experimental Medicine, Saint Petersburg, Russian Federation; email: al.chernov@mail.ru

PY - 2024

Y1 - 2024

N2 - BACKGROUND: Glioblastoma is the most malignant tumor of the central nervous system. Temozolomide is the standard treatment for gliomas, and its use often leads to drug resistance and relapse of glioblastoma. Therefore, further research is needed to find other drugs that can improve the effectiveness of standard treatments. AIM: The goal is to study the effects of nerve growth factor, temozolomide on clonogenicity, migration and energy metabolism of mitochondria of human U251 glioma cells. MATERIALS AND METHODS: The study was conducted on human U251 glioma cells. A colony formation test was used to evaluate the ability of glioma cells to form colonies in vitro. Migration of U251 glioma cells was assessed by the Scratch Assay. To study mitochondrial metabolism in glioma cells, oxygen consumption rate and extracellular acidification rate were measured using the Seahorse XF CellMito and Seahorse XF Glycolysis Stress Test kits, respectively. RESULTS: We found that nerve growth factor (7.55 × 10–3 µM) and temozolomide (155 µM) inhibited the clonoge-nicity of U251 glioma cells by 66.2% and 73.5–81.3% within 1–2 days, respectively. Exposure to nerve growth factor (7.55 × 10–3 µM) also suppresses U251 glioma cell migration on days 3 and 4. Temozolomide (155 µM) inhibits glioma cell migration on days 1–3. The anti-clonogenic and anti-migratory activities of nerve growth factor and temozolomide may be associated with their ability to reduce the basal rate of oxygen consumption, inhibit adenosine triphosphate syn-thetase and maximum mitochondrial respiration in human U251 glioma cells. Nerve growth factor and temozolomide did not affect glycolysis, glycolytic capacity, and glycolytic reserve in U251 glioma cells compared to controls. CONCLUSIONS: Thus, nerve growth factor and temozolomide inhibit migration, clonogenicity, and bioenergetic metabolism of mitochondria in U251 glioma cells, exhibiting anti-mitogenic, anti-migration, and reducing energy metabolism effects. © 2025 Elsevier B.V., All rights reserved.

AB - BACKGROUND: Glioblastoma is the most malignant tumor of the central nervous system. Temozolomide is the standard treatment for gliomas, and its use often leads to drug resistance and relapse of glioblastoma. Therefore, further research is needed to find other drugs that can improve the effectiveness of standard treatments. AIM: The goal is to study the effects of nerve growth factor, temozolomide on clonogenicity, migration and energy metabolism of mitochondria of human U251 glioma cells. MATERIALS AND METHODS: The study was conducted on human U251 glioma cells. A colony formation test was used to evaluate the ability of glioma cells to form colonies in vitro. Migration of U251 glioma cells was assessed by the Scratch Assay. To study mitochondrial metabolism in glioma cells, oxygen consumption rate and extracellular acidification rate were measured using the Seahorse XF CellMito and Seahorse XF Glycolysis Stress Test kits, respectively. RESULTS: We found that nerve growth factor (7.55 × 10–3 µM) and temozolomide (155 µM) inhibited the clonoge-nicity of U251 glioma cells by 66.2% and 73.5–81.3% within 1–2 days, respectively. Exposure to nerve growth factor (7.55 × 10–3 µM) also suppresses U251 glioma cell migration on days 3 and 4. Temozolomide (155 µM) inhibits glioma cell migration on days 1–3. The anti-clonogenic and anti-migratory activities of nerve growth factor and temozolomide may be associated with their ability to reduce the basal rate of oxygen consumption, inhibit adenosine triphosphate syn-thetase and maximum mitochondrial respiration in human U251 glioma cells. Nerve growth factor and temozolomide did not affect glycolysis, glycolytic capacity, and glycolytic reserve in U251 glioma cells compared to controls. CONCLUSIONS: Thus, nerve growth factor and temozolomide inhibit migration, clonogenicity, and bioenergetic metabolism of mitochondria in U251 glioma cells, exhibiting anti-mitogenic, anti-migration, and reducing energy metabolism effects. © 2025 Elsevier B.V., All rights reserved.

KW - clonogenicity

KW - energy metabolism of mitochondria

KW - extracellular acidification rate

KW - human glioma U251

KW - migration

KW - nerve growth factor

KW - oxygen consumption rate

KW - temozolomide

U2 - 10.17816/MAJ632885

DO - 10.17816/MAJ632885

M3 - статья

VL - 24

SP - 109

EP - 123

JO - Medicinskij Akademiceskij Zurnal

JF - Medicinskij Akademiceskij Zurnal

SN - 1608-4101

IS - 4

ER -