ITT Cancer Research – Apoptosis – Oncology

Strongylocentrotus nudos Egg Polysaccharide induces autophagy and apoptosis in leukaemia cells by regulating mitochondrial function

Strongylocentrotus nudos Egg Polysaccharide induces autophagy and apoptosis in leukaemia cells by regulating mitochondrial function

Strongylocentrotus nudos Egg Polysaccharide induces autophagy and apoptosis in leukaemia cells by regulating mitochondrial function

In this study, we investigated the ability of the Polysaccharide from the Eggs of Strongylocentrotus nudus (SEP) to regulate cellular autophagy and apoptosis in leukaemia cells. Human acute myeloid leukaemia (AML) cells (HL60) and murine AML cells (L1210) treated with SEP were used to assess viability using Cell Counting Kit-8, cytotoxicity by measuring lactate dehydrogenase release, the generation of reactive oxygen species (ROS) by DCFH-DA staining. In addition, we utilized a mouse model of leukaemia in which L1210 cells were injected into DBA/2 mice by sub-axillary injection.

Treatment with SEP decreased cell viability, increased in cytotoxicity and increased the release of ROS in a dose-dependent manner. SEP treatment was also associated with the activation of pro-apoptotic proteins cleaved caspase-3, cleaved caspase-9 and cleaved poly (ADP-ribose) polymerase (PARP). Activation of the apoptotic pathway led to the release of cytochrome C (CytoC) into the cytosol of the cell resulting in decreased membrane potential. The effect of SEP treatment was depended on the activation of the nuclear factor kappa-B (NF-κB) signalling pathway as SEP treatment led to an increase in NF-κB phosphorylation, and inhibition of NF-κB signalling using PDTC blocked SEP-mediated activation of apoptosis.

Treatment with SEP also prolonged survival time in our leukaemia mouse model and was associated with diminished tumour volume, increased leucocyte and lymphocyte proliferation, promoted pro-inflammatory factor release in serum and enhanced immune function. Taken together, these data suggest that SEP inhibits the progression of leukaemia by initiating mitochondrial dysfunction, autophagy, and apoptosis via the NF-κB signalling pathway.

 

Microcystin-leucine arginine exposure contributes to apoptosis and follicular atresia in mice ovaries by endoplasmic reticulum stress-upregulated Ddit3

Microcystin-leucine arginine (MC-LR), an intracellular toxin to cause reproduction toxicity, is produced by blooming cyanobacteria and widely distributed in eutrophic waters. It is revealed that MC-LR-induced female reproductive toxicity is more severe than male reproductive toxicity. Previous studies mainly focused on male reproductive toxicity, and the molecular mechanisms of MC-LR-induced apoptosis, follicular atresia and infertility in female remain largely unclear. Here, it was found that MC-LR treatment could induce apoptosis, inflammation, follicular atresia, and decrease of gonadal index in mice ovaries. RNA-Seq data showed that the up-regulation of DNA-damage inducible transcript 3 (Ddit3) under endoplasmic reticulum (ER) stress had predominantly regulatory role in MC-LR-induced apoptotic pathway.
Furthermore, MC-LR exposure promoted cleavage of activating transcription factor 6 (ATF6, 50kd), inositol-requiring enzyme 1 (Ire1) expression, phosphorylation of IRE1, mitogen-activated protein kinase 5 (Map3k5) and Ddit3 expression, which was accompanied by the upregulation of death receptor 5 (Dr5) and active-caspase-3, and a decrease in Bcl-2 expression. ER stress inhibitor 4-Phenyl butyric acid (4-PBA) ameliorated these MC-LR-induced changes in protein or mRNA level. More importantly, knockdown of Ddit3 suppressed MC-LR-induced cell apoptosis and follicular atresia by directly regulating Dr5 and Bcl-2. Additionally, it was also found that MC-LR increased Map3k5 phosphorylation by inhibiting protein phosphatase 2A (PP2A) activity, and then promoted Ddit3 expression. In short, our data suggests that Ddit3 promotes MC-LR-induced mice ovarian cells apoptosis and follicular atresia via ER stress activation, which provides a new insight into the relation between infertility in females and the emerging water pollutant MC-LR.
Strongylocentrotus nudos Egg Polysaccharide induces autophagy and apoptosis in leukaemia cells by regulating mitochondrial function
Strongylocentrotus nudos Egg Polysaccharide induces autophagy and apoptosis in leukaemia cells by regulating mitochondrial function

B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo

Our study was designed to investigate the role of B4GalT1 in glioblastoma, in vitro and in vivo, to detect whether B4GalT1 knockdown could regulate the development of glioblastoma, and further observe the relationship between B4GalT1 knockdown and the apoptosis and autophagy of glioblastoma. To begin, we looked at TCGA and GEPIA systems to predict the potential function of B4GalT1. Western blot and RT-PCR were used to analyze the expression, or mRNA level, of B4GalT1 at different tissue or cell lines. Next, the occurrence and development of glioblastoma, in vitro and in vivo, was observed by using B4GalT1 knocked down by lentivirus. Finally, the apoptosis and autophagy of glioblastoma was observed in vitro and in vivo.

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Description: Goat anti Mouse IgG antibody

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Description: Goat anti Mouse IgG antibody

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Description: Goat anti Mouse IgG secondary antibody

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Description: Goat anti Mouse IgG secondary antibody

Goat anti Mouse IgG

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Description: Goat anti Mouse IgG secondary antibody

Goat anti Mouse IgG

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Description: Goat anti Mouse IgG secondary antibody

Goat Anti Mouse IgG

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Goat Anti-mouse IgG

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Description: Biotinylated goat anti-mouse IgG enables detection of mouse IgG in enzyme immunoassays such as indirect ELISA.

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Description: Goat anti Mouse IgG + IgM secondary antibody

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Description: Goat anti Mouse IgG secondary antibody  (HRP)

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Description: Goat anti Mouse IgG secondary antibody  (FITC)

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Description: Goat anti Mouse IgG secondary antibody  (rhodamine)

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488 Goat-anti-Mouse IgG

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Description: Goat polyclonal to mouse IgG

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Description: Rabbit anti Goat IgG antibody

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Description: Goat anti Cat IgG secondary antibody

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Description: Goat anti Cat IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Goat anti Monkey IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Rabbit anti Goat IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Goat anti Monkey IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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EUR 186
Description: Goat anti Human IgG secondary antibody

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EUR 138
Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Human IgG secondary antibody

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Description: Goat anti Rabbit IgG secondary antibody

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Description: Donkey anti Goat IgG secondary antibody

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Goat anti Rabbit IgG

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Description: Goat anti Rabbit IgG secondary antibody

Goat anti Rabbit IgG

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Description: Goat anti Rabbit IgG secondary antibody

Goat anti Rat IgG

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Description: Goat anti Rat IgG secondary antibody

Goat Anti Human IgG

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Rabbit anti Goat IgG

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goat Anti Rabbit IgG

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Goat anti- human IgG

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  • Recommended dilution: WB: 1:1000-1:10000
  • Immunogen: human IgG
  • Research Area: Immunology
Description: Antibody raised against Goat human IgG

Goat Anti-human IgG

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Description: Biotinylated goat anti-human IgG enables detection of human IgG in enzyme immunoassays such as indirect ELISA.

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Description: Unconjugated Goat monoclonal to Mouse IgG (H+L) antibody

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Description: Unconjugated Goat monoclonal to Mouse IgG (H+L) antibody

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Description: HRP conjugated Goat polyclonal to Mouse IgG (H+L)

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Description: Unconjugated Goat polyclonal to Mouse IgG (H+L)

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EUR 216
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 298
Description: Goat anti Mouse IgG secondary antibody (Fab'2)

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EUR 294
Description: Goat anti Mouse IgG secondary antibody (Fab'2)

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EUR 149
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 137
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 149
Description: Goat anti Mouse IgG (H + L) secondary antibody

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41R-1054 2 mg
EUR 194
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 309
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 153
Description: Goat anti Mouse IgG (H + L) secondary antibody

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EUR 186
Description: Goat anti Mouse IgG (H + L) secondary antibody

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41R-1100 2 mg
EUR 219
Description: Goat anti Mouse IgG (H + L) secondary antibody

Goat anti Mouse IgG (Alk Phos)

43R-1357 1 mg
EUR 224
Description: Goat anti Mouse IgG secondary antibody  (Alk Phos)

Goat anti Mouse IgG Fc (biotin)

43R-1358 2 mg
EUR 224
Description: Goat anti Mouse IgG secondary antibody (biotin)

Goat anti Mouse IgG + IgM (FITC)

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EUR 186
Description: Goat anti Mouse IgG + IgM secondary antibody (FITC)

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EUR 186
Description: Goat anti Mouse IgG + IgM secondary antibody (rhodamine)

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43R-IG051hrp 1 mg
EUR 198
Description: Goat anti Mouse IgG + IgM secondary antibody (HRP)

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EUR 220
Description: Goat anti Mouse IgG secondary antibody (H + L)

Goat Anti-Mouse IgG-Fab, unlabeled

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Goat Anti-Mouse IgG-HRP conjugate

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Goat Anti-Mouse IgG-FITC conjugate

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Results show that B4GalT1 was a highly variable gene, and GEPIA and TCGA systems show B4GalT1 expression in GBM tumor tissue was higher than in normal tissue. Pair-wise gene correlation analysis revealed a probable relationship between B4GalT1 and autophagy related proteins. The B4GalT1 expression and mRNA level were increased in tumor cells, or U87 cells. B4GalT1 knocked down by lentivirus could inhibit glioblastoma development, in vitro and in vivo, by reducing tumor weight and volume, increasing survival, and weakening tumor cells proliferation, migration, invasion. B4GalT1 knockdown could increase apoptosis and autophagy of glioblastoma in vitro and in vivo. Our study demonstrates that B4GalT1 may be able to regulate apoptosis and autophagy of glioblastoma. Bax, Bcl-2, cleaved caspase-3, Beclin-1, and LC3 s may be the downstream target factors of B4GalT1 in apoptosis and autophagy, which may provide a new strategy to reduce glioblastoma development by regulating apoptosis and autophagy.

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