scholarly journals H2O2-Replenishable and GSH-Depletive ROS ‘Bomb’ for Self-Enhanced Chemodynamic Therapy

2021 ◽  
Author(s):  
Fan Zhao ◽  
Jiayu Yao ◽  
Yu Tong ◽  
Dan Su ◽  
Qing Xu ◽  
...  
Keyword(s):  
Hydroxyl Radical ◽  
Tumor Cells ◽  
Tumor Therapy ◽  
Fenton Reagents

Chemodynamic therapy (CDT) is an emerging strategy of tumor therapy which utilizes Fenton reagents to kill tumor cells by disproportionation of H2O2 into hydroxyl radical (•OH). However, insufficient endogenous H2O2...

Nano Technological Approach for Anti-Tumor Therapy: Opportunities and Challenges

2020 ◽  
Vol 10 ◽  
Author(s):  
Krishna Champaneria ◽  
Prajesh Prajapati
Keyword(s):  
Adverse Effects ◽  
Tumor Cells ◽  
Targeted Delivery ◽  
Blood Circulation ◽  
Review Paper ◽  
Tumor Therapy ◽  
Conventional Chemotherapy ◽  
Targeting Delivery ◽  
Tumor Accumulation ◽  
Work Done

Cancer is one of the reason for mortality and its individual and collective impact is substantial. Conventional chemotherapy utilizes drugs that can destroy Tumor cells effectively. But these agents destroy healthy cells along with the tumor cells, leading to many adverse effects which include hypersensitivity reactions, nephrotoxicity, and neurotoxicity. To minimize the adverse effects, various drug delivery systems (DDSs) has been developed. Among them, nanoparticles are attractive platforms for it. So this review paper explores the recent work done on targeted delivery, enhancing tumor accumulation and longer blood circulation using more effective biomaterial that will enhance the properties of nanoparticles. Moreover, various target-specific delivery of drugs like antibody-targeted, targeting delivery through angiogenesis, mitochondria, CD44 receptor are also explained.

scholarly journals Epigenetic Targeting of Autophagy via HDAC Inhibition in Tumor Cells: Role of p53

2018 ◽  
Vol 19 (12) ◽  
pp. 3952 ◽  
Author(s):  
Maria Mrakovcic ◽  
Lauren Bohner ◽  
Marcel Hanisch ◽  
Leopold F. Fröhlich
Keyword(s):  
Cell Death ◽  
Tumor Cells ◽  
Histone Deacetylase ◽  
Stress Responses ◽  
Histone Deacetylase Inhibitors ◽  
Tumor Therapy ◽  
Regulatory System ◽  
Anticancer Activities ◽  
Mutational Status

Tumor development and progression is the consequence of genetic as well as epigenetic alterations of the cell. As part of the epigenetic regulatory system, histone acetyltransferases (HATs) and deacetylases (HDACs) drive the modification of histone as well as non-histone proteins. Derailed acetylation-mediated gene expression in cancer due to a delicate imbalance in HDAC expression can be reversed by histone deacetylase inhibitors (HDACi). Histone deacetylase inhibitors have far-reaching anticancer activities that include the induction of cell cycle arrest, the inhibition of angiogenesis, immunomodulatory responses, the inhibition of stress responses, increased generation of oxidative stress, activation of apoptosis, autophagy eliciting cell death, and even the regulation of non-coding RNA expression in malignant tumor cells. However, it remains an ongoing issue how tumor cells determine to respond to HDACi treatment by preferentially undergoing apoptosis or autophagy. In this review, we summarize HDACi-mediated mechanisms of action, particularly with respect to the induction of cell death. There is a keen interest in assessing suitable molecular factors allowing a prognosis of HDACi-mediated treatment. Addressing the results of our recent study, we highlight the role of p53 as a molecular switch driving HDACi-mediated cellular responses towards one of both types of cell death. These findings underline the importance to determine the mutational status of p53 for an effective outcome in HDACi-mediated tumor therapy.

From Antimicrobial to Anticancer Peptides: The Transformation of Peptides

2019 ◽  
Vol 14 (1) ◽  
pp. 70-84 ◽  
Author(s):  
Yuan Qin ◽  
Zuo D. Qin ◽  
Jing Chen ◽  
Che G. Cai ◽  
Ling Li ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Tumor Cells ◽  
Tumor Therapy ◽  
Relevant Literature ◽  
Point Of View ◽  
Research Trend ◽  
Gram Positive Bacteria ◽  
Anticancer Peptides ◽  
Search Data ◽  
Tumor Drugs

Background: Antimicrobial peptides play an important role in the innate immune system. Possessing broad-spectrum antibacterial activity, antimicrobial peptides can quickly treat and kill various targets, including gram-negative bacteria, gram-positive bacteria, fungi, and tumor cells.Objective:An overview of the state of play with regard to the research trend of antimicrobial peptides in recent years and the situation of targeting tumor cells, and to make statistical analysis of the patents related to anticancer peptides published in recent years, is important both from toxicological and medical tumor therapy point of view.Methods:Based on the Science Citation Index Expanded version, the Derwent Innovation Index and Innography as data sources, the relevant literature and patents concerning antimicrobial peptides and anticancer peptides were analyzed through the Thomson Data Analyzer. Results of toxicologic and pharmacologic studies that brought to the development of patents for methods to novel tumor drugs were analyzed and sub-divided according to the specific synthesis of anticancer peptides.Results:The literature and patent search data show that the research and development of global antimicrobial peptides and anticancer peptides has been in an incremental mode. Growing patent evidence indicate that bioinformatics technology is a valuable strategy to modify, synthesize or recombine existing antimicrobial peptides to obtain tumor drugs with high activity, low toxicity and multiple targets.Conclusion:These findings may have important clinical implications for cancer treatment, especially in patients with conditions that are not currently treatable by other drugs, or that are resistant to existing cancer drugs.

scholarly journals Bifunctional, Copper-Doped, Mesoporous Silica Nanosphere-Modified, Bioceramic Scaffolds for Bone Tumor Therapy

2020 ◽  
Vol 8 ◽  
Author(s):  
Hongshi Ma ◽  
Zhenjiang Ma ◽  
Qufei Chen ◽  
Wentao Li ◽  
Xiangfei Liu ◽  
...  
Keyword(s):  
Mesoporous Silica ◽  
Tumor Cells ◽  
Bone Tumor ◽  
Checkpoint Inhibitors ◽  
Tumor Therapy ◽  
Residual Tumor ◽  
Bone Defects ◽  
Silica Nanosphere ◽  
Large Bone ◽  
Large Bone Defects

In the traditional surgical intervention procedure, residual tumor cells may potentially cause tumor recurrence. In addition, large bone defects caused by surgery are difficult to self-repair. Thus, it is necessary to design a bioactive scaffold that can not only kill residual tumor cells but also promote bone defect regeneration simultaneously. Here, we successfully developed Cu-containing mesoporous silica nanosphere-modified β-tricalcium phosphate (Cu-MSN-TCP) scaffolds, with uniform and dense nanolayers with spherical morphology via 3D printing and spin coating. The scaffolds exhibited coating time- and laser power density-dependent photothermal performance, which favored the effective killing of tumor cells under near-infrared laser irradiation. Furthermore, the prepared scaffolds favored the proliferation and attachment of rabbit bone marrow-derived mesenchymal stem cells and stimulated the gene expression of osteogenic markers. Overall, Cu-MSN-TCP scaffolds can be considered for complete eradication of residual bone tumor cells and simultaneous healing of large bone defects, which may provide a novel and effective strategy for bone tumor therapy. In the future, such Cu-MSN-TCP scaffolds may function as carriers of anti-cancer drugs or immune checkpoint inhibitors in chemo-/photothermal or immune-/photothermal therapy of bone tumors, favoring for effective treatment.

scholarly journals Transdifferentiation mediated tumor suppression by the endoplasmic reticulum stress sensor IRE-1 in C. elegans

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Mor Levi-Ferber ◽  
Hai Gian ◽  
Reut Dudkevich ◽  
Sivan Henis-Korenblit
Keyword(s):  
Tumor Cell ◽  
Er Stress ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Tumor Therapy ◽  
Tumor Model ◽  
Apoptosis Resistance ◽  
Stress Sensor ◽  
C Elegans ◽  
Cell Transdifferentiation

Deciphering effective ways to suppress tumor progression and to overcome acquired apoptosis resistance of tumor cells are major challenges in the tumor therapy field. We propose a new concept by which tumor progression can be suppressed by manipulating tumor cell identity. In this study, we examined the effect of ER stress on apoptosis resistant tumorous cells in a Caenorhabditis elegans germline tumor model. We discovered that ER stress suppressed the progression of the lethal germline tumor by activating the ER stress sensor IRE-1. This suppression was associated with the induction of germ cell transdifferentiation into ectopic somatic cells. Strikingly, transdifferentiation of the tumorous germ cells restored their ability to execute apoptosis and enabled their subsequent removal from the gonad. Our results indicate that tumor cell transdifferentiation has the potential to combat cancer and overcome the escape of tumor cells from the cell death machinery.

Human U3 protein 14a plays an anti-apoptotic role in cancer cells

2017 ◽  
Vol 398 (11) ◽  
pp. 1247-1257 ◽  
Author(s):  
Teng Ma ◽  
Chenxi Lu ◽  
Yafei Guo ◽  
Chunfeng Zhang ◽  
Xiaojuan Du
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Protein Level ◽  
Tumor Therapy ◽  
Caspase Inhibitor ◽  
Chemotherapeutic Drug ◽  
Intrinsic Pathway ◽  
Down Regulation ◽  
Drug Induced ◽  
Induced Apoptosis

AbstractHuman U three protein 14a (hUTP14a) binds p53 and promotes p53 degradation. Here, we report that hUTP14a plays an anti-apoptotic role in tumor cells through a p53-independent pathway. Knockdown of hUTP14a activated the intrinsic pathway of apoptosis and sensitized tumor cells to chemotherapeutic drug-induced apoptosis. In addition, the protein level of hUTP14a decreased upon chemotherapeutic drug- or irradiation-induced apoptosis. Importantly, the decrease of hUTP14a during induced apoptosis was not blocked by pan-caspase inhibitor z-VAD-FMK, indicating that the down-regulation of hUTP14a is an upstream event in apoptosis. Furthermore, ectopically expressed hUTP14a protected tumor cells from chemotherapeutic drug-induced apoptosis. In summary, our data showed that hUTP14a protected tumor cells from chemotherapeutic drug-induced apoptosis and thus might possess a potential as a target for anti-tumor therapy.

scholarly journals Targeting Mitochondrial Metabolism and RNA Polymerase POLRMT to Overcome Multidrug Resistance in Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Hui-Jing Yu ◽  
Guan-Li Xiao ◽  
Yu-Ying Zhao ◽  
Xin-Xin Wang ◽  
Rongfeng Lan
Keyword(s):  
Multidrug Resistance ◽  
Rna Polymerase ◽  
Tumor Cells ◽  
Energy Supply ◽  
Mitochondrial Gene ◽  
Tumor Therapy ◽  
Tca Cycle ◽  
Mitochondrial Metabolism ◽  
Mitochondrial Rna ◽  
Clinical Issue

Clinically, the prognosis of tumor therapy is fundamentally affected by multidrug resistance (MDR), which is primarily a result of enhanced drug efflux mediated by channels in the membrane that reduce drug accumulation in tumor cells. How to restore the sensitivity of tumor cells to chemotherapy is an ongoing and pressing clinical issue. There is a prevailing view that tumor cells turn to glycolysis for energy supply due to hypoxia. However, studies have shown that mitochondria also play crucial roles, such as providing intermediates for biosynthesis through the tricarboxylic acid (TCA) cycle and a plenty of ATP to fuel cells through the complete breakdown of organic matter by oxidative phosphorylation (OXPHOS). High OXPHOS have been found in some tumors, particularly in cancer stem cells (CSCs), which possess increased mitochondria mass and may be depends on OXPHOS for energy supply. Therefore, they are sensitive to inhibitors of mitochondrial metabolism. In view of this, we should consider mitochondrial metabolism when developing drugs to overcome MDR, where mitochondrial RNA polymerase (POLRMT) would be the focus, as it is responsible for mitochondrial gene expression. Inhibition of POLRMT could disrupt mitochondrial metabolism at its source, causing an energy crisis and ultimately eradicating tumor cells. In addition, it may restore the energy supply of MDR cells to glycolysis and re-sensitize them to conventional chemotherapy. Furthermore, we discuss the rationale and strategies for designing new therapeutic molecules for MDR cancers by targeting POLRMT.

scholarly journals In vivo induction of terminal differentiation of malignant myelopoietic progenitor cells by CSF-inducing biological response modifiers

Blood ◽  
1986 ◽  
Vol 67 (4) ◽  
pp. 980-987
Author(s):  
E Schlick ◽  
FW Ruscetti
Keyword(s):  
Bone Marrow ◽  
Tumor Cells ◽  
Tumor Therapy ◽  
Terminal Differentiation ◽  
Biological Response ◽  
Biological Response Modifiers ◽  
Therapeutic Effects ◽  
Antitumor Effects ◽  
Tumor Bearing

We have investigated the mechanisms by which colony-stimulating factor (CSF)-inducing biological response modifiers (BRM) may have beneficial effects on tumor-bearing hosts undergoing anti-tumor therapy. First, we have documented that treatment of mice with the chemically defined BRM maleic anhydride divinyl ether copolymer (MVE-2), which induces CSF secretion by macrophages (M phi) and bone marrow cells (BMC), significantly increased growth and differentiation of normal myelopoietic cells and counteracted the myelosuppressive effects of cyclophosphamide (CY). Second, we established that MVE-2 may exert CSF- mediated antitumor effects on certain leukemic tumor cells. Serum from mice pretreated in vivo with MVE-2, which contained CSF, induced terminal differentiation of cloned tumor cells from the CSF responsive WEHI-3B D+ subline in vitro, but not from the WEHI-3B D- subline, which is unresponsive to CSF. In vivo experiments showed that treatment of mice bearing the WEHI-3B D+ tumor first with CY and three days later with the CSF inducer MVE-2, significantly increased their survival time and rendered 20% to 50% of the tumor-bearing mice disease free. No such effects were obtained in mice bearing the WEHI-3B D- tumor. Thus, the induction of CSF or other differentiation factors by some BRMs may result in therapeutic effects against certain leukemias based on at least two distinct mechanisms: In addition to their restorative effects on normal bone marrow functions, CSF-inducing BRMs may also prevent further leukemogenesis by induction of terminal differentiation of leukemic cells.

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