Hydrogen peroxide induces programmed cell death features in cultured tobacco BY-2 cells, in a dose-dependent manner

This study investigated the effect of CAPE on planktonic growth, biofilm-forming abilities, mature biofilms, and cell death of C. albicans, C. tropicalis, C. glabrata, and C. parapsilosis strains. Our results showed a strain- and dose-dependent effect of CAPE on Candida, and the MIC values were between 12.5 and 100 µg/mL. Similarly, the MBIC values of CAPE ranging between 50 and 100 µg/mL highlighted the inhibition of the biofilm-forming abilities in a dose-dependent manner, as well. However, CAPE showed a weak to moderate biofilm eradication ability (19-49%) on different Candida strains mature biofilms. Both caspase-dependent and caspase-independent apoptosis after CAPE treatment were observed in certain tested Candida strains. Our study has displayed typical apoptotic hallmarks of CAPE-induced chromatin margination, nuclear blebs, nuclear condensation, plasma membrane detachment, enlarged lysosomes, cytoplasm fragmentation, cell wall distortion, whole-cell shrinkage, and necrosis. In conclusion, CAPE has a concentration and strain-dependent inhibitory activity on viability, biofilm formation ability, and cell death response in the different Candida species.

Download Full-text

TB-4 Antitumor effects of a novel curcumin derivative curcumin monoglucuronide on glioblastoma cells in vitro and in vivo

Neuro-Oncology Advances ◽

10.1093/noajnl/vdab159.022 ◽

2021 ◽

Vol 3 (Supplement_6) ◽

pp. vi6-vi6

Author(s):

Takashi Fujii ◽

Shun Yamamuro ◽

Masamichi Takahashi ◽

Akihide Kondo ◽

Yoshitaka Narita ◽

...

Keyword(s):

Cell Death ◽

Water Soluble ◽

Dependent Manner ◽

Antitumor Effects ◽

Multiple Cell ◽

Human Gbm ◽

Dose Dependent ◽

Novel Therapeutic

Abstract The therapeutic outcome of glioblastomas (GBMs) is still very poor. Therefore, invention of novel therapeutic methods against GBM cases is considered urgent. The antitumor effects of naturally-derived compounds are attracting attention recently, and therapeutic efficacy of curcumin, a plant-derived compound previously used for multiple purpose, has been indicated in many cancer systems; however, clinical application of curcumin is considered difficult because of its poor bioavailability (under 1 %). Curcumin monoglucuronide (CMG), a water-soluble prodrug of curcumin recently developed for overcoming this weakness, has been demonstrated excellent antitumor effects for several malignancies in vitro and in vivo; therefore, we investigated the effects of CMG against GBM cells. CMG induced cell death of human GBM cells lines (T98G, U251MG, and U87MG) by dose dependent manner by triggering multiple forms of cell death such as apoptosis and perthanatos. Immunoblotting of CMG-treated GBM cell lysates demonstrated activation of multiple cell death signaling. Furthermore, immunodeficiency mice harboring intracerebral U87MG cell xenografts systemically treated by CMG showed significantly prolonged survival compared with control mice. These results suggest CMG would be a novel therapeutic agent against GBM cases.

Download Full-text

Hydrogen peroxide as a signal controlling plant programmed cell death

The Journal of Cell Biology ◽

10.1083/jcb.200409170 ◽

2005 ◽

Vol 168 (1) ◽

pp. 17-20 ◽

Cited By ~ 316

Author(s):

Tsanko S. Gechev ◽

Jacques Hille

Keyword(s):

Hydrogen Peroxide ◽

Cell Death ◽

Programmed Cell Death ◽

Signaling Pathways ◽

Microarray Analysis ◽

Plant Cell ◽

Full Genome ◽

Genome Coverage ◽

Regulatory Mutants

Hydrogen peroxide (H2O2) has established itself as a key player in stress and programmed cell death responses, but little is known about the signaling pathways leading from H2O2 to programmed cell death in plants. Recently, identification of key regulatory mutants and near-full genome coverage microarray analysis of H2O2-induced cell death have begun to unravel the complexity of the H2O2 network. This review also describes a novel link between H2O2 and sphingolipids, two signals that can interplay and regulate plant cell death.

Download Full-text

Glucose oxidase prevents programmed cell death of the silkworm anterior silk gland through hydrogen peroxide production

FEBS Journal ◽

10.1111/j.1742-4658.2010.07996.x ◽

2011 ◽

Vol 278 (5) ◽

pp. 776-785 ◽

Cited By ~ 7

Author(s):

Hiroto Matsui ◽

Motonori Kakei ◽

Masafumi Iwami ◽

Sho Sakurai

Keyword(s):

Hydrogen Peroxide ◽

Cell Death ◽

Programmed Cell Death ◽

Glucose Oxidase ◽

Silk Gland ◽

Hydrogen Peroxide Production

Download Full-text

Enhanced Malignant Phenotypes of Glioblastoma Cells Surviving NPe6-Mediated Photodynamic Therapy are Regulated via ERK1/2 Activation

Cancers ◽

10.3390/cancers12123641 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3641

Author(s):

Tatsuya Kobayashi ◽

Makoto Miyazaki ◽

Nobuyoshi Sasaki ◽

Shun Yamamuro ◽

Eita Uchida ◽

...

Keyword(s):

Cell Death ◽

Photodynamic Therapy ◽

Migration And Invasion ◽

Dependent Manner ◽

Potential Therapeutic Target ◽

Talaporfin Sodium ◽

Polymerase Inhibitor ◽

Human Gbm ◽

Dose Dependent

To manage refractory and invasive glioblastomas (GBM)s, photodynamic therapy (PDT) using talaporfin sodium (NPe6) (NPe6-PDT) was recently approved in clinical practice. However, the molecular machineries regulating resistance against NPe6-PDT in GBMs and mechanisms underlying the changes in GBM phenotypes following NPe6-PDT remain unknown. Herein, we established an in vitro NPe6-mediated PDT model using human GBM cell lines. NPe6-PDT induced GBM cell death in a NPe6 dose-dependent manner. However, this NPe6-PDT-induced GBM cell death was not completely blocked by the pan-caspase inhibitor, suggesting NPe6-PDT induces both caspase-dependent and -independent cell death. Moreover, treatment with poly (ADP-ribose) polymerase inhibitor blocked NPe6-PDT-triggered caspase-independent GBM cell death. Next, it was also revealed resistance to re-NPe6-PDT of GBM cells and GBM stem cells survived following NPe6-PDT (NPe6-PDT-R cells), as well as migration and invasion of NPe6-PDT-R cells were enhanced. Immunoblotting of NPe6-PDT-R cells to assess the behavior of the proteins that are known to be stress-induced revealed that only ERK1/2 activation exhibited the same trend as migration. Importantly, treatment with the MEK1/2 inhibitor trametinib reversed resistance against re-NPe6-PDT and suppressed the enhanced migration and invasion of NPe6-PDT-R cells. Overall, enhanced ERK1/2 activation is suggested as a key regulator of elevated malignant phenotypes of GBM cells surviving NPe6-PDT and is therefore considered as a potential therapeutic target against GBM.

Download Full-text