Requirement for ERK Activity in Sodium Selenite-induced Apoptosis of Acute Promyelocytic Leukemia-derived NB4 Cells

Han, Bingshe; Wei, Wei; Hua, Fangyuan; Cao, Tingming; Dong, Hua; Yang, Tao; Yang, Yang; Pan, Huazhen; Xu, Caimin

doi:10.5483/bmbrep.2007.40.2.196

Cited by 31 publications

(26 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All-trans retinoic acid (ATRA) and arsenic trioxide have been successful in treating APL, but both drugs have some limitations [15,16]. In previous studies, we discovered that 20 lM sodium selenite markedly inhibited the proliferation and induced apoptosis of NB4 cells in a time-dependent manner [17,18]. In the present study, we further investigated the molecular mechanisms by which 20 lM sodium seleniteinduced apoptosis in NB4 cells.…”

Section: Introductionmentioning

confidence: 78%

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

Guan

Han

et al. 2009

Apoptosis

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 78%

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

Guan

Han

et al. 2009

Apoptosis

Self Cite

View full text Add to dashboard Cite

show abstract

“…The activation of this pathway allows cells to inhibit apoptotic and autophagic programmed cell death, which may contribute to malignant transformation and tumor growth (11)(12)(13). Moreover, activated Akt also stimulates the mTOR/P70S6-kinase pathway, whose activation is required for the initiation of protein synthesis (14,15).…”

Section: Introductionmentioning

confidence: 99%

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

Ren¹,

Huang²,

Liu³

et al. 2009

BMB Reports

Self Cite

View full text Add to dashboard Cite

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]

show abstract

“…Another known oxidative stress-induced response pathway comprises so-called MAPKs whose three main members -ERK, JNK and p38 -were reported to be implicated in selenite-induced cell injury and cell death [18,22,23]. Our data demonstrate time-dependent significant activation of p38 and JNK kinases; however with different timing.…”

Section: Discussionmentioning

confidence: 44%

ROS mediate selenite-induced apoptosis in colon cancer cells

2010

View full text Add to dashboard Cite

Selenite-induced oxidative stress and its relationship to mitochondrial apoptosis was studied in human adenocarcinoma HT-29 cells.It is shown that selenite induces caspase-dependent apoptosis, which is mediated by mitochondria via released cytochrome c, apoptosis-inducing factor (AIF) and Smac/Diablo. Selenite activates stress kinases p38 and JNK while suppressing reduced glutathione (GSH) and thioredoxin reductase (TrxR) levels, transiently inducing heme oxygenase (HO-1) system as well as reducing Akt expression. Pre-treatment of cells with selected antioxidants and stress kinase inhibitors significantly prevented selenite-induced cell death, thereby implicating oxidative stress as a direct (Bax)

show abstract

Requirement for ERK Activity in Sodium Selenite-induced Apoptosis of Acute Promyelocytic Leukemia-derived NB4 Cells

Cited by 31 publications

References 13 publications

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

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

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

ROS mediate selenite-induced apoptosis in colon cancer cells

Contact Info

Product

Resources

About