Sublethal concentrations of high glucose prolong mitotic arrest in a spindle assembly checkpoint activity dependent manner in budding yeast
Küçük Resim Yok
Tarih
2021
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Springer
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
The most successful anti-cancer drugs in clinical use interfere with cell cycle progression by inducing a mitotic arrest through activation of a conserved surveillance mechanism called the spindle assembly checkpoint (SAC). Cancer cells require much more glucose compared to normal cells to meet their energy needs due to reprogramming of their energy metabolism. Therefore, hyperglycemia may be favorable for cancer cells. Indeed, hyperglycemia is known to be closely associated with increased risk of developing several types of cancers as well as cancer related-mortality. However, the effect of hyperglycemic conditions on the mitotic arrest induced by anti-cancer drugs remains unknown. In this study, we investigated the effect of incubation in high glucose containing media on the duration of mitotic arrest induced by a SAC-activating anti-cancer drug, nocodazole, in budding yeast. We first showed that high glucose led to cell death in a dose and time dependent manner in yeast. Next, we examined the effect of sublethal concentrations of high glucose on nocodazole-induced mitotic arrest. Our data revealed that high glucose prolongs nocodazole induced mitotic arrest. Finally, we investigated whether the delay observed in exiting from nocodazole-induced mitotic arrest requires SAC activity. For this purpose, we induced a mitotic arrest that is independent of SAC activation and showed that the delay in exiting from nocodazole-induced mitotic arrest required SAC activity.
Açıklama
Anahtar Kelimeler
Spindle Assembly Checkpoint, Mitotic Arrest, High Glucose, Cancer, Saccharomyces Cerevisiae
Kaynak
Biologia
WoS Q Değeri
Q3
Scopus Q Değeri
Q3
Cilt
76
Sayı
12
