Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.4.2.30 (PARP)
 13,611 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anticancer efficiencies and mechanisms of Pheophorbide-a-mediated photodynamic, sonodynamic and sonophotodynamic therapies were investigated in vitro using androgen-sensitive (LNCaP) and androgen insensitive (PC3) prostate cancer cell lines. The cells were incubated in RPMI-1640 media at various concentrations of Pheophorbide-a. The media was treated with 0.5 W/cm2 ultrasound and/or 0.5 mJ/cm2 light irradiation. Cell proliferation in both cell lines was inhibited most effectively by sonophotodynamic therapy in comparison to that of both monotherapies. LNCaP cells were more sensitive to the applied treatments and the cell survival in LNCaP cell line was observed to be less than that of PC3 cell line. The results of histochemical analysis showed that there were more apoptotic cells in the treatment groups in comparison to control group. Additionally, the treatments induced apoptosis deduced by the overexpressed levels of caspase-3, caspase-8, PARP, and Bax proteins, while the expression levels of caspase-9 and Bcl-2 proteins were observed to be lower than those of control group. Treatments led to an increase in the oxidative stress markers, ROS and MDA, but a decrease in the activities of antioxidant enzymes, SOD, CAT and GSH. The results of this study revealed that Pheophorbide a-mediated sonophotodynamic therapy more efficiently activates the apoptotic mechanisms in prostate cancer cells and thus may provide a promising approach for treatment.
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PMID:Pheophorbide a-mediated sonodynamic, photodynamic and sonophotodynamic therapies against prostate cancer. 3261 16

The immunodeficiency observed in HIV-1-infected patients is mainly due to uninfected bystander CD4+ T lymphocyte cell death. The viral envelope glycoproteins (Env), expressed at the surface of infected cells, play a key role in this process. Env triggers macroautophagy/autophagy, a process necessary for subsequent apoptosis, and the production of reactive oxygen species (ROS) in bystander CD4+ T cells. Here, we demonstrate that Env-induced oxidative stress is responsible for their death by apoptosis. Moreover, we report that peroxisomes, organelles involved in the control of oxidative stress, are targeted by Env-mediated autophagy. Indeed, we observe a selective autophagy-dependent decrease in the expression of peroxisomal proteins, CAT and PEX14, upon Env exposure; the downregulation of either BECN1 or SQSTM1/p62 restores their expression levels. Fluorescence studies allowed us to conclude that Env-mediated autophagy degrades these entire organelles and specifically the mature ones. Together, our results on Env-induced pexophagy provide new clues on HIV-1-induced immunodeficiency. Abbreviations: Ab: antibodies; AF: auranofin; AP: anti-proteases; ART: antiretroviral therapy; BafA1: bafilomycin A1; BECN1: beclin 1; CAT: catalase; CD4: CD4 molecule; CXCR4: C-X-C motif chemokine receptor 4; DHR123: dihydrorhodamine 123; Env: HIV-1 envelope glycoproteins; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GFP-SKL: GFP-serine-lysine-leucine; HEK: human embryonic kidney; HIV-1: type 1 human immunodeficiency virus; HTRF: homogeneous time resolved fluorescence; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; NAC: N-acetyl-cysteine; PARP: poly(ADP-ribose) polymerase; PEX: peroxin; ROS: reactive oxygen species; siRNA: small interfering ribonucleic acid; SQSTM1/p62: sequestosome 1.
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PMID:HIV-1 Env induces pexophagy and an oxidative stress leading to uninfected CD4+ T cell death. 3307 73


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