Escitalopram oxalate induces apoptosis in U-87MG cells and autophagy in GBM8401 cells.
Vincent Chin-Hung ChenYi-Hsien HsiehLi-Jeng ChenTsai-Ching HsuBor-Show TzangPublished in: Journal of cellular and molecular medicine (2017)
Glioblastoma multiforme (GBM) is recognized as a most aggressive brain cancer with the worst prognosis and survival time. Owing to the anatomic location of gliomas, surgically removing the tumour is very difficult and avoiding damage to vital brain regions during radiotherapy is impossible. Therefore, therapeutic strategies for malignant glioma must urgently be improved. Recent studies have demonstrated that selective serotonin reuptake inhibitors (SSRIs) have cytotoxic effect on certain cancers. Considering as a more superior SSRI, escitalopram oxalate exhibits favourable tolerability and causes generally mild and temporary adverse events. However, limited information is revealed about the influence of escitalopram oxalate on GBM. Therefore, an attempt was made herein to explore the effects of escitalopram oxalate on GBM. The experimental results revealed that escitalopram oxalate significantly inhibits the proliferation and invasive ability of U-87MG cells and significantly reduced the expressions of cell cycle inhibitors such as Skp2, P57, P21 and P27. Notably, escitalopram oxalate also induced significant apoptotic cascades in U-87MG cells and autophagy in GBM8401 cells. An animal study indicated that escitalopram oxalate inhibits the proliferation of xenografted glioblastoma in BALB/c nude mice. These findings implied that escitalopram oxalate may have potential in treatment of glioblastomas.
Keyphrases
- induced apoptosis
- major depressive disorder
- cell cycle arrest
- cell death
- cell cycle
- signaling pathway
- endoplasmic reticulum stress
- oxidative stress
- healthcare
- squamous cell carcinoma
- multiple sclerosis
- cell proliferation
- single cell
- resting state
- social media
- high glucose
- functional connectivity
- high grade
- smoking cessation
- papillary thyroid
- diabetic rats
- cerebral ischemia
- climate change
- lymph node metastasis