Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells

Abstract

(2010) Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells, Autophagy,6:6,[711][712][713][714][715][716][717][718][719][720][721][722][723][724]

Quercetin induces protective autophagy in gastric cancer cells: Involvement of Akt-mTOR- and hypoxia-induced factor 1α-mediated signaling

“…Certain anticancer agents i.e., polyoxomolybdates-, platonin-or phenethyl isothiocyanate could induce autophagic cell death to enhance chemotherapeutic efficacy, [41][42][43] while others, i.e., suberoylanilide hydroxamic acid, arginine deiminase or timosaponin A-III mediated protective autophagy that antagonized apoptotic cell death. [31][32][33] In this study, we demonstrated that quercetin triggered autophagy in human gastric cancer cells both in vitro and in vivo. Further functional analysis showed that inhibition of autophagy markedly increased quercetin-induced apoptotic cell death, suggesting that quercetin-induced autophagy plays a protective role in gastric cancer cells.…”

“…Accumulating evidence suggested a paradoxical role of autophagy in control of cell death and survival under various stimulus conditions. [31][32][33][34][35][36] To determine the in the cytoplasm of both AGS and MKN28 cells treated with quercetin. To further characterize the membrane-associated vacuoles, acridine orange staining was used to analyze the formation of acidic vesicular organelles (AVOs), a main feature of autophagy.…”

Suberoylanilide hydroxamic acid (SAHA) causes tumor growth slowdown and triggers autophagy in glioblastoma stem cells

“…39 Further experiments with acridine orange and MDC staining also confirmed SAHA-induced autophagy in GSCs, similar to results of studies on hepatocellular carcinoma and T-leukemia cells. 21,22 A possible explanation for the increase in SAHA-mediated autophagy-induction is that SAHA inactivates AKT-MTOR signaling by dephosphorylation of Ser473 and MTOR Ser2448. Depletion of autophagy-related genes or pharmacological inhibition resulted in SAHA-induced apoptosis at the early phase, whereas cotreatment of rapamycin provided a protective effect against the activation of caspase by overdose induction of SAHA treatment, suggesting that SAHAinduced autophagy functions as a prosurvival mechanism to mitigate SAHA-induced apoptotic cell death.…”

“…Several studies have suggested that SAHA could induce autophagy in certain types of cancers, including hepatocellular carcinoma and T-leukemia cells, 21,22 and we hypothesized that SAHA causes autophagy in GSCs. Transmission electron microscopy (TEM) is a standard method to reliably detect autophagy.…”

“…To detect the development of AVOs, we treated GSCs as described above and then performed vital staining with acridine orange as described previously. 22 Briefly, the treated adherent GSCs or differentiated GSCs were stained with acridine orange (1 μg/ml) for 15 min. Samples were examined under a fluorescence microscope.…”