Proteomics analysis of A375 human malignant melanoma cells in response to arbutin treatment

Nawarak, Jiraporn; Liu, Rosa Huang; Kao, Shao‐Hsuan; Liao, Hung-Ju; Sinchaikul, Supachok; Chen, Shui‐Tein; Cheng, Sun-Long

doi:10.1016/j.bbapap.2008.09.023

Cited by 54 publications

(46 citation statements)

References 54 publications

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“…4), it is possible that the enhancement of VDAC oligomerization caused by apoptosis inducers might result from the upregulation of the VDAC expression level. Indeed, it has been shown previously, using gene microarray techniques, that irradiation of apoptosis-sensitive cells, which typically induces apoptosis, caused strong VDAC upregulation (56), while a proteomics-based investigation of the anticancer effects of arbutin on A375 cells also found that the VDAC was upregulated (35). However, under on May 12, 2018 by guest http://mcb.asm.org/ the conditions used in this study to induce apoptosis, we observed no increase in VDAC expression levels as determined by Western blot analysis (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, small interfering RNA (siRNA)-mediated downregulation of VDAC1 expression prevented cisplatin-induced Bax activation; strongly reduced the cisplatininduced release of Cyto c and AIF, as well as the maturation of caspase-3 (51); and attenuated endostatin-induced apoptosis (60). Finally, overexpression of human, murine, yeast, and rice VDAC1 was found to induce apoptotic cell death, regardless of the cell type used (3,19,61), while arbutin (hydroquinone-O-␤-D-glucopyranoside) induced apoptosis by inducing VDAC1 overexpression (35). On the other hand, VDAC proteins have been reported to be dispensable for Ca 2ϩ -and oxidative-stress-induced permeability transition pore (PTP) opening (10).…”

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confidence: 99%

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Oligomerization of the Mitochondrial Protein Voltage-Dependent Anion Channel Is Coupled to the Induction of Apoptosis

Keinan

Tyomkin

Shoshan‐Barmatz

2010

Molecular and Cellular Biology

217

246

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Accumulating evidence implicates that the voltage-dependent anion channel (VDAC) functions in mitochondrion-mediated apoptosis and as a critical player in the release of apoptogenic proteins, such as cytochrome c, triggering caspase activation and apoptosis. The mechanisms regulating cytochrome c release and the molecular architecture of the cytochrome c-conducting channel remain unknown. Here the relationship between VDAC oligomerization and the induction of apoptosis was examined. We demonstrated that apoptosis induction by various stimuli was accompanied by highly increased VDAC oligomerization, as revealed by cross-linking and directly monitored in living cells using bioluminescence resonance energy transfer technology. VDAC oligomerization was induced in all cell types and with all apoptosis inducers used, including staurosporine, curcumin, As 2 O 3 , etoposide, cisplatin, selenite, tumor necrosis factor alpha (TNF-␣), H 2 O 2 , and UV irradiation, all acting through different mechanisms yet all involving mitochondria. Moreover, correlation between the levels of VDAC oligomerization and apoptosis was observed. Furthermore, the apoptosis inhibitor 4,4-diisothiocyanostilbene-2,2-disulfonic acid (DIDS) inhibited VDAC oligomerization. Finally, a caspase inhibitor had no effect on VDAC oligomerization and cytochrome c release. We propose that VDAC oligomerization is involved in mitochondrion-mediated apoptosis and may represent a general mechanism common to numerous apoptogens acting via different initiating cascades. Thus, targeting the oligomeric status of VDAC, and hence apoptosis, offers a therapeutic strategy for combating cancers and neurodegenerative diseases.It is well accepted that mitochondria serve as integrators and amplifiers of programmed cell death through the regulation of apoptosis, mediating the release of proapoptotic proteins and/or disrupting cellular energy metabolism (25). During the transduction of an apoptotic signal into the cell, an alteration in mitochondrial membrane permeability occurs, facilitating the release of apoptogenic proteins, such as cytochrome c (Cyto c), apoptosis-inducing factor (AIF), and Smac/DIABLO, from the intermembrane space into the cytosol (45). These proteins participate in complex processes resulting in the activation of proteases and nucleases, leading to protein and DNA degradation and, ultimately, cell death (25). However, it remains unclear how these apoptotic initiators cross the outer mitochondrial membrane (OMM) and are released into the cytosol. While some models predict that such release is facilitated by swelling of the mitochondrial matrix and subsequent rupture of the OMM, other models predict the formation of protein-conducting channels that are large enough to allow the passage of Cyto c and other proteins into the cytosol without compromising OMM integrity (15,44,47). The voltage-dependent anion channel (VDAC) offers such a route (45).Located in the OMM, the VDAC forms the main interface between the mitochondrial and cellular metabolisms by medi...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Oligomerization of the Mitochondrial Protein Voltage-Dependent Anion Channel Is Coupled to the Induction of Apoptosis

Keinan

Tyomkin

Shoshan‐Barmatz

2010

Molecular and Cellular Biology

217

246

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“…5 The molecular weights of the proteins were distributed within the range of 25 to 97 kDa, and the differentially expressed protein spots had isoelectric points distributed between acidic and basic pH 29 . Using PDQuest image analysis software, approximately 540 spots were found in the control and treatment groups with no significant difference between the groups.…”

Section: -D Page Of A375 Melanoma Cells Following Arbutin Treatmentmentioning

confidence: 99%

“…Using the MASCOT protein identification search software for identifying both PMF and MS/MS ion mass data, 26 differentially expressed proteins were successfully identified 29 . Among these proteins, there were five up-regulated and 15 down-regulated proteins (including their isoforms).…”

Section: Identification Of Differentially Expressed Proteinsmentioning

confidence: 99%

Molecular Profiling of A375 Human Malignant Melanoma Cells Treated with Kojic Acid and Arbutin

Hsieh¹,

Chen²,

Cheng³

2011

Breakthroughs in Melanoma Research

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“…Overexpression of VDAC from multiple different sources ranging from yeast to human induces apoptotic cell death, suggesting that VDAC is a universally conserved mitochondrial element of PCD in eukaryotic systems (Godbole et al, 2003;Zaid et al, 2005;Ghosh et al, 2007;Lu et al, 2007). Although VDAC expression levels appear to be critical for mitochondria-mediated PCD (Voehringer et al, 2000;Castagna et al, 2004;Nawarak et al, 2009), the mechanism underlying cell death induced by VDAC overexpression remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Genomic survey and gene expression analysis of the VDAC gene family in rice

Xu¹,

Tan²,

Cheng³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The voltage-dependent anion channel (VDAC), also known as a mitochondrial porin, plays an important role in the regulation of metabolic and energetic functions of mitochondria, as well as in mitochondria-mediated apoptosis. Cytoplasmic male sterility (CMS) is of major economic importance for commercial hybrid production and a research model for the interaction between nuclear and cytoplasmic genomes. Recent research has revealed that CMS is associated with programmed cell death. Here, we used the Honglian (HL)-CMS line of rice (Oryza sativa) as material to investigate the association of O. sativa VDAC (OsVDAC) expression to CMS. Eight VDACs were extracted from rice in this study. Bioinformatic analysis of the rice VDACs was conducted at the DNA, cDNA, and protein level. Expression patterns of OsVDACs were analyzed in different organs and during different stages of pollen development using sterile line YuetaiA (YTA), and its maintainer line YuetaiB (YTB). Differential expression of OsVDACs between YTA and YTB was observed, suggesting that VDACs may be involved in the formation of HL-CMS.

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Proteomics analysis of A375 human malignant melanoma cells in response to arbutin treatment

Cited by 54 publications

References 54 publications

Oligomerization of the Mitochondrial Protein Voltage-Dependent Anion Channel Is Coupled to the Induction of Apoptosis

Oligomerization of the Mitochondrial Protein Voltage-Dependent Anion Channel Is Coupled to the Induction of Apoptosis

Molecular Profiling of A375 Human Malignant Melanoma Cells Treated with Kojic Acid and Arbutin

Genomic survey and gene expression analysis of the VDAC gene family in rice

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