scholarly journals Recent Advancements in Apoptosis-Based Therapeutic Approaches for Cancer Targeting

2021 ◽  
Author(s):  
Mehmet Evren Okur ◽  
Panoraia I. Siafaka ◽  
Merve Tutar ◽  
Yusuf Tutar
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Anticancer Drugs ◽  
Anticancer Agents ◽  
Scientific Community ◽  
Polymer Nanoparticles ◽  
Cancer Targeting ◽  
Therapeutic Approaches ◽  
Induction Of Apoptosis

Apoptosis, known as programmed cell death, has been considered a potent target for the pharmacy industry. The scientific community has actively participated to research which evaluate active molecules for possible inhibition or induction of apoptosis. Nanocarriers especially for cancer targeting are widely found through literature; they mainly based on inorganic, lipid or polymer nanoparticles which incorporate anticancer drugs. Another important and innovative category of anticancer agents is that of microRNAs. In this chapter, a discussion about the most recent applications of apoptosis-based agents mainly focusing on cancer target is done.

Activation of programmed cell death (apoptosis) by cisplatin, other anticancer drugs, toxins and hyperthermia

1990 ◽  
Vol 40 (10) ◽  
pp. 2353-2362 ◽  
Author(s):  
Michael A. Barry ◽  
Catherine A. Behnke ◽  
Alan Eastman
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Anticancer Drugs

scholarly journals Rapid induction of apoptosis by deregulated uptake of polyamine analogues

1997 ◽  
Vol 328 (1) ◽  
pp. 307-316 ◽  
Author(s):  
Rei-Huang HU ◽  
E. Anthony PEGG
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Oxidation Products ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Polyamine Biosynthesis ◽  
Polyamine Analogues ◽  
Induction Of Apoptosis

Treatment of Chinese hamster ovary cells with α-difluoromethylornithine for 3 days, followed by exposure to cycloheximide, led to an unregulated, rapid and massive accumulation of polyamine analogues. This accumulation led to cell death by apoptosis within a few hours. Clear evidence of DNA fragmentation was seen in response to both N-terminally ethylated polyamines and to polyamines containing methyl groups on the terminal carbon atoms. Programmed cell death was induced within 2-4 h of exposure to 1 μM or higher concentrations of N1,N11-bis(ethyl)norspermine. The presence of cycloheximide increased the uptake of the polyamine analogues and therefore led to cell death at lower analogue concentrations, but it was not essential for the induction of apoptosis, since similar effects were seen when the protein synthesis inhibitor was omitted and the concentration of N1,N11-bis(ethyl)norspermine was increased to 5 μM or more The induction of apoptosis was blocked both by the addition of the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, or by the addition of the polyamine oxidase inhibitor N1-methyl-N2-(2,3-butadienyl)butane-1,4-diamine (MDL 72,527). These experiments provide evidence to support the concepts that: (1) polyamines or their oxidation products may be initiators of programmed cell death; (2) regulation of polyamine biosynthesis and uptake prevents the accumulation of toxic levels of polyamines; and (3) the anti-neoplastic effects of bis(ethyl) polyamine analogues may be due to the induction of apoptosis in sensitive tumour cells.

scholarly journals In vivo induction of apoptosis (programmed cell death) in mouse thymus by administration of lipopolysaccharide.

1993 ◽  
Vol 61 (12) ◽  
pp. 5044-5048 ◽  
Author(s):  
Y H Zhang ◽  
K Takahashi ◽  
G Z Jiang ◽  
M Kawai ◽  
M Fukada ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mouse Thymus ◽  
Induction Of Apoptosis ◽  
In Vivo Induction

Loss of sphingosine kinase‐1 activates the intrinsic pathway of programmed cell death: modulation of sphingolipid levels and the induction of apoptosis

2005 ◽  
Vol 20 (3) ◽  
pp. 482-484 ◽  
Author(s):  
Tarek A. Taha ◽  
Kazuyuki Kitatani ◽  
Mazen El‐Alwani ◽  
Jacek Bielawski ◽  
Yusuf A. Hannun ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Sphingosine Kinase ◽  
Sphingosine Kinase 1 ◽  
Intrinsic Pathway ◽  
Induction Of Apoptosis

scholarly journals Programmed cell death proteins and chronic leukemia

2011 ◽  
Vol 63 (3) ◽  
pp. 527-535
Author(s):  
G. Brajuskovic ◽  
Milica Strnad ◽  
Snezana Cerovic ◽  
Stanka Romac
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Chronic Leukemia ◽  
Morphological Aspects ◽  
Pathological Conditions ◽  
Wide Range ◽  
Induction Of Apoptosis ◽  
Apoptotic Genes

Apoptosis or programmed cell death is a genetically regulated process of cellular suicide. Apoptosis has been implicated in a wide range of pathological conditions, and mutations in apoptotic genes play important roles in the process of malignant transformation. Chronic leukemia represents a neoplastic disorder caused primarily by defective programmed cell death, as opposed to increased cell proliferation. This paper presents the main results of our ten-year research on the apoptosis of leukemia cells. The research included the morphological aspects of the process, the effect of antineoplastic agents on the induction of apoptosis in leukemia cells and expression analysis of the proteins involved in programmed cell death. Special attention was paid to the expression and interaction of the Bcl-2 family of proteins in leukemia cells. The ultimate aim of the study of apoptosis of leukemic cells is the discovery of new biological agents that might be used in the treatment of chronic leukemia.

scholarly journals Iridium(III) Complexes Targeting Apoptotic Cell Death in Cancer Cells

Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2739 ◽  
Author(s):  
Dik-Lung Ma ◽  
Chun Wu ◽  
Ke-Jia Wu ◽  
Chung-Hang Leung
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Anticancer Agents ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Lower Toxicity ◽  
Cisplatin Analogues

Targeting apoptosis is a principal strategy in the design of anticancer drugs. In recent years, non-platinum-based scaffolds have been exploited as viable candidates for the exploitation of anticancer agents with potentially lower toxicity than the widely used cisplatin analogues. This review highlights the latest advances in developing iridium(III) complexes as anticancer agents that act particularly via targeting apoptotic cell death in cancer cells.

B-cell–specific transcription factor BACH2 modifies the cytotoxic effects of anticancer drugs

Blood ◽  
2003 ◽  
Vol 102 (9) ◽  
pp. 3317-3322 ◽  
Author(s):  
Takuya Kamio ◽  
Tsutomu Toki ◽  
Rika Kanezaki ◽  
Shinya Sasaki ◽  
Satoru Tandai ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Anticancer Drugs ◽  
Anticancer Agents ◽  
Philadelphia Chromosome ◽  
Lymphoid Cells ◽  
Chromosome 1 ◽  
Nuclear Accumulation ◽  
Cytotoxic Effects

AbstractThe transcription factor Bach2, a member of the CNC family of proteins, binds to the Maf recognition element (MARE) by forming homodimers or dimerizing with small Maf transcription factors. Bach2-expressing cells show reduced proliferation and undergo spontaneous cell death. The inhibition of BCR/ABL tyrosine kinase activity by STI571 in chronic myeloid leukemia (CML) cell lines and CD34+ cells from patients with CML in lymphoid crisis results in induction of BACH2 expression. We show here that BACH2 modifies the in vitro cytotoxicity of anticancer drugs. The cytotoxic effects of commonly used anticancer agents were studied by overexpression of BACH2 in RAJI lymphoid cells, a cell line that does not express endogenous BACH2. Cell growth inhibition was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Clones overexpressing BACH2 were more sensitive to etoposide, doxorubicin, and cytarabine than control RAJI cells, whereas there were no significant differences in the sensitivity of either cells to methotrexate or vincristine. Interestingly, we found that the former drugs were oxidative stressors that induced the nuclear accumulation of BACH2. In contrast, methotrexate or vincristine did not induce production of intracellular reactive oxygen species (ROS) and nuclear accumulation of BACH2. These results, coupled with our previous data showing that BACH2 promotes oxidative stress-induced cell death, suggest that combination chemotherapy involving STI571 and anticancer drugs that produce ROS may be of benefit in the treatment of Philadelphia chromosome 1 (Ph1)–positive leukemia.

scholarly journals Integrated analysis of programmed cell death ligand 1 expression reveals increased levels in high-grade glioma

2021 ◽  
Author(s):  
Dorothee Hölzl ◽  
Georg Hutarew ◽  
Barbara Zellinger ◽  
Hans U. Schlicker ◽  
Christoph Schwartz ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immunohistochemical Analysis ◽  
High Grade Glioma ◽  
Integrated Analysis ◽  
Therapeutic Approaches ◽  
Who Grade ◽  
L1 Protein ◽  
Promoter Mutations ◽  
Opening Up

Abstract Purpose Gliomas are the most frequent primary brain tumors of adults. Despite intensive research, there are still no targeted therapies available. Here, we performed an integrated analysis of glioma and programmed cell death ligand 1 (PD-L1) in 90 samples including 58 glioma and 32 control brain tissues. Methods To identify PD-L1 expression in glioma, we performed immunohistochemical analysis of PD-L1 tumor proportion score (TPS) using the clinically valid PD-L1 22C3 antibody on 90 samples including controls and WHO grade I–IV gliomas. Results We found that PD-L1 is highly expressed in a subfraction of glioma cells. Analysis of PD-L1 levels in different glioma subtypes revealed a strong intertumoral variation of PD-L1 protein. Furthermore, we correlated PD-L1 expression with molecular glioma hallmarks such as MGMT-promoter methylation, IDH1/2 mutations, TERT promoter mutations and LOH1p/19q. Conclusion In summary, we found that PD-L1 is highly expressed in a subfraction of glioma, indicating PD-L1 as a potential new marker in glioma assessment opening up novel therapeutic approaches.

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