Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells

Guan, Lina; Han, Binshe; Li, Zhushi; Hua, Fangyuan; Huang, Fang; Wei, Wei; Yang, Yang; Xu, Caimin

doi:10.1007/s10495-008-0295-5

Cited by 90 publications

(75 citation statements)

References 34 publications

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“…Moreover, activated Akt also stimulates the mTOR/P70S6-kinase pathway, whose activation is required for the initiation of protein synthesis (14,15). Our former studies showed that the expression of p-Akt, down-stream factor of PI3K, decreased in selenite induced apoptosis in NB4 cells (16). Consequently, we postulated that the PI3K pathway plays an important role in the inhibition of autophagy and the increase of apoptosis in NB4 cells.…”

Section: Introductionmentioning

confidence: 83%

Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells

Ren¹,

Huang²,

Liu³

et al. 2009

BMB Reports

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Selenium possesses the chemotherapeutic feature by inducing apoptosis in cancer cell with trivial side effects on normal cells. However, the mechanism in which is not clearly understood. Emerging evidence indicates the overlaps between the autophagy and the apoptosis. In this study, we have investigated the role of autophagy in selenium-induced apoptosis in NB4 cells. We find that autophagy is suppressed in NB4 cells treated by sodium selenite, as measured by electron microscope, acridine orange staining and western blot. Moreover, selenite combined with autophagy inhibitor contributes to the up-regulation of apoptosis, while the PI3K/Akt signaling pathway is down-regulated. Consistently, when the inhibitor of PI3K was applied, the autophagic level significantly decreased. In summary, sodium selenite increases NB4 cell apoptosis by autophagy inhibition through PI3K/Akt, and the inhibition of autophagy contributes to the up-regulation of apoptosis. [BMB reports 2009; 42(9): 599-604]

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Section: Introductionmentioning

confidence: 83%

Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells

Ren¹,

Huang²,

Liu³

et al. 2009

BMB Reports

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“…Previous studies indicated that the antitumor activity of selenium compounds was often attributed to drug-induced apoptosis (5,6,20). Here we addressed that autophagy acted as another essential mechanism for the application of selenite in cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidences confirmed the application of selenite in studies of cell proliferation and cancer (3,4). Previous results suggested supranutritional doses of selenite promoted cell death through mitochondria-or ER stress-mediated apoptotic pathway in human leukemia cell lines (5,6). Furthermore, autophagy has recently been considered as an alternative mechanism of cell death induced by selenite, which caused concurrence of autophagy and apoptosis in leukemia cells (7,8).…”

Section: Introductionmentioning

confidence: 87%

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Jiang

Li²,

Shi³

et al. 2012

BMB Reports

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Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at Ser 308. We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at Ser 308 serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise. [BMB reports 2012; 45(3): [194][195][196][197][198][199]

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“…cells by the generation of reactive oxygen species (ROS) [24]. In addition, many organic/inorganic selenium compounds have been found capable of inducing apoptotic death of tumour cells [25,26].…”

Section: Introductionmentioning

confidence: 99%

Dual functional selenium-substituted hydroxyapatite

Wang

Zhou

et al. 2012

Interface Focus.

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Hydroxyapatite (HA) doped with trace elements has attracted much attention recently owing to its excellent biological functions. Herein, we use a facile co-precipitation method to incorporate selenium into HA by adding sodium selenite during synthesis. The obtained selenium-substituted HA products are needle-like nanoparticles which have size and crystallinity that are similar to those of the pure HA nanoparticles (HANs) when the selenium content is low. HANs are found to have the ability to induce the apoptosis of osteosarcoma cells, and the anti-tumour effects are enhanced after incorporation of selenium. Meanwhile, the nanoparticles can also support the growth of bone marrow stem cells. Furthermore, the flow cytometric results indicate that the apoptosis induction of osteosarcoma cells is caused by the increased reactive oxygen species and decreased mitochondrial membrane potential. These results show that the selenium-substituted HANs are potentially promising bone graft materials in osteosarcoma treatment due to their dual functions of supporting normal cell growth and inducing tumour cell apoptosis.

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Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells

Abstract: Sodium selenite-induced reactive oxygen species generation is an early event that triggers endoplasmic reticulum stress mitochondrial apoptotic pathways in NB4 cells.

Cited by 90 publications

References 34 publications

Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells

Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Dual functional selenium-substituted hydroxyapatite

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