Bid Stands at the Crossroad of Stress-Response Pathways

Song, Gang; Chen, G.G.; Hu, Tianming; Lai, Paul B.S.

doi:10.2174/156800910791859515

Cited by 28 publications

(33 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the extrinsic pathway, caspase-8 activation in turn leads directly to activation of caspase-3 and thus apoptosis [30,48]. Moreover, once cleaved by caspase-8, truncated Bid can migrate to the mitochondria where it can initiate the intrinsic pathway and activate caspase-9 [32]. We provided evidence that DD1 treatment induced caspase-8 activation, but not Bid truncation, in U937 cells.…”

Section: Discussionmentioning

confidence: 72%

See 1 more Smart Citation

p70S6 kinase is a target of the novel proteasome inhibitor 3,3′-diamino-4′-methoxyflavone during apoptosis in human myeloid tumor cells

Piedfer

Bouchet

Tang

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

Acute myeloid leukemia (AML) is a deadly disease characterized by the clonal expansion and accumulation of hematopoietic stem cells arrested at various stages of development. Clinical research efforts are currently focusing on targeted therapies that induce apoptosis in AML cells. Herein, the effects and mechanisms of the novel flavone 3,3'-diamino-4'-methoxyflavone (DD1) on AML cell dysfunction were investigated in AML cells (monoblast U937, myelomonocyte OCI-AML3, promyelocyte NB4, myeloblast HL-60) and blood samples from patients with AML. The administration of DD1 inhibited proliferation and induced death of AML cell lines and reduced the clonogenic activity of AML, but not normal, blood cells. The flavone's apoptotic action in U937 cells was associated with recruitment of mitochondria, Bax activation, Bad dephosphorylation (at Ser(136)), activation of caspases -8, -9, and -3 and cleavage of the caspase substrate PARP-1. DD1 induced a marked decrease in (i) Thr(389)-phosphorylation and (ii) protein levels of the caspase-3 substrate P70 ribosomal S6 kinase (P70S6K, known for its ability to phosphorylate Bad). Caspase-dependent apoptosis and P70S6K degradation were simultaneously prevented by the caspase inhibitors. Importantly, DD1 was shown to directly inhibit the proteasome's chymotrypsin-like activity in U937 cells. Apoptotic activity of the proteasome inhibitor bortezomib was also related to Bax activation and P70S6K downregulation. Accordingly, DD1 failed to induce P70S6K cleavage, Bax stimulation and apoptosis in K562 cells resistant to bortezomib. These results indicate that DD1 has the potential to eradicate AML cells and support a critical role for Bax and P70S6K in DD1-mediated proteasome inhibition and apoptosis of leukemia cells.

show abstract

Section: Discussionmentioning

confidence: 72%

“…5B,C). Bid is a known caspase substrate and the production of truncated Bid (tBid) can activate the intrinsic pathway of apoptosis [32]. Untreated U937 cells expressed high levels of Bid and DD1 treatment did not lead to either loss of intact Bid (Fig.…”

Section: Dd1 Induces Mitochondrial Membrane Depolarization Bax Upregmentioning

confidence: 99%

p70S6 kinase is a target of the novel proteasome inhibitor 3,3′-diamino-4′-methoxyflavone during apoptosis in human myeloid tumor cells

Piedfer

Bouchet

Tang

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

show abstract

“…Subsequently, caspase-9 is activated, leading to the induction of apoptosis in the cells. 37,38 As shown in Figure 4C, Bid and Bcl-2 activity decreased and Bax increased in HT-29 cells following the addition of membrane proteins from heat-killed L. plantarum L67. We assumed that the membrane proteins blocked survival factors such as Bid and Bcl-2 but induced caspase-8 and caspase-3 activity.…”

Section: Discussionmentioning

confidence: 91%

The proteins (12 and 15 kDa) isolated from heat‐killed Lactobacillus plantarum L67 induces apoptosis in HT‐29 cells

Song

Lim

2015

Cell Biochemistry & Function

View full text Add to dashboard Cite

A number of scientific studies have revealed that Lactobacillus strains have beneficial bioactivities in the gastrointestinal tract. In this study, the production of intracellular reactive oxygen species (ROS) and the amounts of intracellular calcium, protein kinase C activity, cytochrome c, Bid, Bcl-2, Bax and the apoptosis-mediated proteins [caspase-8, caspase-3 and poly ADP ribose polymerase (PARP)] were evaluated to understand the induction of programmed cell death in HT-29 cells by Lactobacillus plantarum L67. The results obtained from this study indicated that the relative intensities of the apoptotic-related factors (intracellular ROS and intracellular calcium) and of apoptotic signals (Bax and t-Bid) increased with increasing concentrations of the membrane proteins isolated from heat-killed L. plantarum L67, whereas the relative intensities of cytochrome c, Bcl-2, caspase-8, caspase-3 and PARP decreased. This study determines whether proteins (12 and 15 kDa) isolated from heat-killed L. plantarum L67 induce programmed cell death in HT-29 cells. Proteins isolated from L. plantarum L67 can stimulate the apoptotic signals and then consequently induce programmed cell death in HT-29 cells. The results in this study suggest that the proteins isolated from L. plantarum L67 could be used as an antitumoural agent in probiotics and as a component of supplements or health foods.

show abstract

“…In this complex, proteolytic cleavage of procaspase-8 occurs, followed by cleavage of two critical exogenous apoptotic substrates, caspase-3 and Bid protein. Bid protein, pro-death Bcl-2 family protein member is activated by cleavage by caspase-8 and other proteases, couples the death receptor pathway to the mitochondria-initiated, intrinsic apoptotic pathway (Song et al 2010). This pathway may be triggered by both external and internal stimuli and is characterized by mitochondrial membrane depolarization, the release of cytochrome c and other proapoptotic factors from mitochondria, and activation of caspase-9 at the apoptosome (Riedl and Salvesen 2007).…”

Section: Proapoptotic Effect Of Hgfmentioning

confidence: 99%

Paradoxical action of growth factors: antiproliferative and proapoptotic signaling by HGF/c-MET

Grzelakowska-Sztabert

Dudkowska

2011

Growth Factors

View full text Add to dashboard Cite

Hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (c-MET) signaling is usually associated with the promotion of cellular growth and often with progression of tumors. Nevertheless, under certain conditions HGF can also act as an antiproliferative and proapoptotic factor and can sensitize various cancer cells, treated with anticancer drugs, to apoptosis. Not only HGF but also its various truncated forms as well as intracellular fragments of its membrane receptor, c-MET, may act as antiproliferative and proapoptotic factors toward various cells. This review focuses on different mechanisms responsible for such paradoxical action of the known typical growth factor. It also points toward the possibilities of usage of this information in anticancer therapy.

show abstract

Bid Stands at the Crossroad of Stress-Response Pathways

Cited by 28 publications

References 0 publications

p70S6 kinase is a target of the novel proteasome inhibitor 3,3′-diamino-4′-methoxyflavone during apoptosis in human myeloid tumor cells

p70S6 kinase is a target of the novel proteasome inhibitor 3,3′-diamino-4′-methoxyflavone during apoptosis in human myeloid tumor cells

The proteins (12 and 15 kDa) isolated from heat‐killed Lactobacillus plantarum L67 induces apoptosis in HT‐29 cells

Paradoxical action of growth factors: antiproliferative and proapoptotic signaling by HGF/c-MET

Contact Info

Product

Resources

About