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  6. Keywords
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We are analyzing https://link.springer.com/article/10.1007/s10495-007-0052-1.

Title:
Lysosomal and mitochondrial pathways in miltefosine-induced apoptosis in U937 cells | Apoptosis
Description:
Hexadecylphosphocholine (HePC) is an anticancer agent whose effect has been shown to involve apoptosis induction but the signaling pathways leading to apoptosis remain to be elucidated. We show here that HePC induces activation of caspase-9, -3, and -8 via the intrinsic pathway, release of cytochrome c, activation and relocation of Bax to the mitochondria as well as the cleavage of Bid. Moreover, a lysosomal pathway characterized by partial lysosomal rupture, cathepsin B activation and relocation from lysosomes to the cytosol, is involved in HePC-induced apoptosis. A cathepsin B/L inhibitor partially suppresses caspase activation and apoptosis induction, indicating signaling between lysosomes and mitochondria. Conversely, the pancaspase inhibitor Q-VD-OPH inhibits lysosomal rupture, but only at early time points, suggesting that immediate lysosomal rupture involves caspases. Overexpression of Bcl-2, an anti-apoptotic protein known to prevent mitochondrial dysfunction, totally abrogates lysosomal destabilization and cell death.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

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Keywords {🔍}

google, scholar, article, pubmed, cas, apoptosis, cell, death, lysosomal, mitochondrial, cells, cancer, anticancer, pathways, hexadecylphosphocholine, bcl, van, activation, res, caspase, cathepsin, lysosomes, access, biol, induction, pathway, bax, mitochondria, human, gajate, phospholipid, miltefosine, chem, kroemer, privacy, cookies, content, cleavage, mollinedo, ether, eibl, exp, membrane, pharmacol, publish, search, paris, bertoglio, bréard, bid,

Topics {✒️}

ether phospholipid 1-o-octadecyl-2-o-methyl-rac-glycero-3-phosphocholine month download article/chapter anti-cancer alkyl-lysophospholipids inhibit jacques bertoglio & jacqueline bréard apaf-1/caspase-9 complex initiates mitochondrial dysfunction-dependent mechanisms enhance radiation-induced apoptosis miltefosine-induced apoptosis monitored erucylphosphocholine-induced apoptosis depends dna damage-induced apoptosis related subjects fas receptor/ligand system skin-metastasized breast cancer full article pdf human leukemic cells human leukemia cells datp-dependent formation article apoptosis aims partial lysosomal rupture radiation-induced apoptosis privacy choices/manage cookies miltefosine-induced apoptosis miltefosine induced apoptosis erucylphosphocholine-induced apoptosis antitumor ether phospholipid caspase-3-dependent tumor cell lines ceramide-mediated apoptosis membrane phospholipid metabolism signal transduction mediated hepc-induced apoptosis prevent mitochondrial dysfunction providing financial support lysosomal pathway characterized anticancer phospholipid analog activate mitochondrial apoptosis hexadecylphosphocholine inhibits translocation check access instant access u937 cells published etherphospholipid analogue hexadecylphosphocholine alkyl-lysophospholipids activate lysosomal membrane permeabilization anti-apoptotic protein caspase-3 protease family article paris atractyloside-induced release sapk/jnk pathway toxic proteins released target cells leads

Questions {❓}

  • Kagedal K, Johansson AC, Johansson U et al (2005) Lysosomal membrane permeabilization during apoptosis—involvement of Bax?
  • Vander Heiden MG, Thompson CB (1999) Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis?

Schema {🗺️}

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         headline:Lysosomal and mitochondrial pathways in miltefosine-induced apoptosis in U937 cells
         description:Hexadecylphosphocholine (HePC) is an anticancer agent whose effect has been shown to involve apoptosis induction but the signaling pathways leading to apoptosis remain to be elucidated. We show here that HePC induces activation of caspase-9, -3, and -8 via the intrinsic pathway, release of cytochrome c, activation and relocation of Bax to the mitochondria as well as the cleavage of Bid. Moreover, a lysosomal pathway characterized by partial lysosomal rupture, cathepsin B activation and relocation from lysosomes to the cytosol, is involved in HePC-induced apoptosis. A cathepsin B/L inhibitor partially suppresses caspase activation and apoptosis induction, indicating signaling between lysosomes and mitochondria. Conversely, the pancaspase inhibitor Q-VD-OPH inhibits lysosomal rupture, but only at early time points, suggesting that immediate lysosomal rupture involves caspases. Overexpression of Bcl-2, an anti-apoptotic protein known to prevent mitochondrial dysfunction, totally abrogates lysosomal destabilization and cell death.
         datePublished:2007-03-09T00:00:00Z
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      headline:Lysosomal and mitochondrial pathways in miltefosine-induced apoptosis in U937 cells
      description:Hexadecylphosphocholine (HePC) is an anticancer agent whose effect has been shown to involve apoptosis induction but the signaling pathways leading to apoptosis remain to be elucidated. We show here that HePC induces activation of caspase-9, -3, and -8 via the intrinsic pathway, release of cytochrome c, activation and relocation of Bax to the mitochondria as well as the cleavage of Bid. Moreover, a lysosomal pathway characterized by partial lysosomal rupture, cathepsin B activation and relocation from lysosomes to the cytosol, is involved in HePC-induced apoptosis. A cathepsin B/L inhibitor partially suppresses caspase activation and apoptosis induction, indicating signaling between lysosomes and mitochondria. Conversely, the pancaspase inhibitor Q-VD-OPH inhibits lysosomal rupture, but only at early time points, suggesting that immediate lysosomal rupture involves caspases. Overexpression of Bcl-2, an anti-apoptotic protein known to prevent mitochondrial dysfunction, totally abrogates lysosomal destabilization and cell death.
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