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

Jiang, Qian; Li, Feng; Shi, Kejian; Yang, Yang; Xu, Caimin

doi:10.5483/bmbrep.2012.45.3.194

Cited by 23 publications

(13 citation statements)

References 29 publications

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“…Jiang et al . documented that sodium selenite‐induced activation of DAPK promotes autophagy. In our early study, we also found a positive role of DAPK in autophagy induction, as SB203580, a pyridinyl imidazole, induced autophagy via activating DAPK to maintain the survival of HCC cells .…”

Section: Discussionmentioning

confidence: 99%

“…Kiyono et al [24] reported that transforming growth factor-beta activated autophagy to tender its growth inhibitory effect on tumour cells. Jiang et al [25] documented that sodium selenite-induced activation of DAPK promotes autophagy. In our early study, we also found a positive role of DAPK in autophagy induction, as SB203580, a pyridinyl imidazole, induced autophagy via activating DAPK to maintain the survival of HCC cells [11].…”

Section: Discussionmentioning

confidence: 99%

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Hepatitis B virus x protein induces autophagy via activating death‐associated protein kinase

Zhang

Chen

et al. 2013

Journal of Viral Hepatitis

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Hepatitis B virus x protein (HBX), a product of hepatitis B virus (HBV), is a multifunctional protein that regulates viral replication and various cellular functions. Recently, HBX has been shown to induce autophagy; however, the responsible mechanism is not fully known. In this study, we established stable HBX-expressing epithelial Chang cells as the platform to study how HBX induced autophagy. The results showed that the overexpression of HBX resulted in starvation-induced autophagy. HBX-induced autophagy was related to its ability to dephosphorylate/activate death-associated protein kinase (DAPK). The block of DAPK by its siRNA significantly counteracted HBX-mediated autophagy, confirming the positive role of DAPK in this process. HBX also induced Beclin 1, which functions at the downstream of the DAPK-mediated autophagy pathway. Although HBX could activate JNK, a kinase known to participate in autophagy in certain conditions, the change in JNK failed to influence HBX-induced autophagy. In conclusion, HBX induces autophagy via activating DAPK in a pathway related to Beclin 1, but not JNK. This new finding should help us to understand the role of autophagy in HBX-mediated pathogenesis and thus may provide targets for intervening HBX-related disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus x protein induces autophagy via activating death‐associated protein kinase

Zhang

Chen

et al. 2013

Journal of Viral Hepatitis

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“…1 Recently, autophagy has been recognized as a cell death mechanism that takes place in various types of cancer cells in response to anticancer therapies. 2 …”

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confidence: 99%

A ginseng metabolite, compound K, induces autophagy and apoptosis via generation of reactive oxygen species and activation of JNK in human colon cancer cells

et al. 2013

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Compound K (20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol) is an active metabolite of ginsenosides and induces apoptosis in various types of cancer cells. This study investigated the role of autophagy in compound K-induced cell death of human HCT-116 colon cancer cells. Compound K activated an autophagy pathway characterized by the accumulation of vesicles, the increased positive acridine orange-stained cells, the accumulation of LC3-II, and the elevation of autophagic flux. Whereas blockade of compound K-induced autophagy by 3-methyladenein and bafilomycin A1 significantly increased cell viability. In addition, compound K augmented the time-dependent expression of the autophagy-related proteins Atg5, Atg6, and Atg7. However, knockdown of Atg5, Atg6, and Atg7 markedly inhibited the detrimental impact of compound K on LC3-II accumulation and cell vitality. Compound K-provoked autophagy was also linked to the generation of intracellular reactive oxygen species (ROS); both of these processes were mitigated by the pre-treatment of cells with the antioxidant N-acetylcysteine. Moreover, compound K activated the c-Jun NH2-terminal kinase (JNK) signaling pathway, whereas downregulation of JNK by its specific inhibitor SP600125 or by small interfering RNA against JNK attenuated autophagy-mediated cell death in response to compound K. Compound K also provoked apoptosis, as evidenced by an increased number of apoptotic bodies and sub-G1 hypodiploid cells, enhanced activation of caspase-3 and caspase-9, and modulation of Bcl-2 and Bcl-2-associated X protein expression. Notably, compound K-stimulated autophagy as well as apoptosis was induced by disrupting the interaction between Atg6 and Bcl-2. Taken together, these results indicate that the induction of autophagy and apoptosis by compound K is mediated through ROS generation and JNK activation in human colon cancer cells.

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“…9 In addition, reports using other cell lines have shown that selenite promotes both autophagy and apoptosis. 10, 11, 12, 13 On the basis of these previous studies, elucidating the relationship between autophagy and apoptosis in cancer cells after selenite exposure is necessary.…”

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confidence: 99%

Survivin-2B promotes autophagy by accumulating IKK alpha in the nucleus of selenite-treated NB4 cells

Shi

Shan

et al. 2014

Cell Death Dis

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Survivin-2B, a known splice variant of survivin, has been reported to promote cell death in some cancer cells, although it keeps prosurvival function in others, and the mechanisms are unclear. In this report, we discovered that selenite, an antitumor agent, switched protective autophagy to apoptosis in NB4 cells. In this process, the level of survivin-2B was decreased and the interaction between IKK alpha and survivin-2B in the nucleus was attenuated, which further led to the decrease of nuclear IKK alpha. As a result, P73, a known transcript factor of UVRAG, was downregulated. Therefore, the expression of UVRAG, one of the initiators of autophagy, was inhibited. The regulatory status of survivin-2B was also proved in NB4 cells after different chemicals' exposure and in other tumor cell lines (Jurkat, HCT116). Finally, experiments in vivo confirmed that the alterations of survivin-2B, IKK alpha, P73 and UVRAG were the same as that in vitro. Taken together, survivin-2B promoted autophagy and further regulated cell death by accumulating and stabilizing IKK alpha in the nucleus.

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

Cited by 23 publications

References 29 publications

Hepatitis B virus x protein induces autophagy via activating death‐associated protein kinase

Hepatitis B virus x protein induces autophagy via activating death‐associated protein kinase

A ginseng metabolite, compound K, induces autophagy and apoptosis via generation of reactive oxygen species and activation of JNK in human colon cancer cells

Survivin-2B promotes autophagy by accumulating IKK alpha in the nucleus of selenite-treated NB4 cells

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