scholarly journals ANTITUMOR EFFECT OF ELECTROMAGNETIC FIELDS AND THEIR EFFECT ON PAIN IN EXPERIMENTAL AND CLINICAL ONCOLOGY

2019 ◽  
Vol 6 (2) ◽  
pp. 86-99 ◽  
Author(s):  
E. M. Frantsiyants ◽  
E. A. Sheiko
Keyword(s):  
Tumor Cells ◽  
Electromagnetic Fields ◽  
Analgesic Effect ◽  
Electromagnetic Waves ◽  
Antitumor Effect ◽  
Living Organism ◽  
Inhibitory Effect ◽  
Chemotherapeutic Agents ◽  
Scientific Publications

The review examined and analyzed scientific publications on the effect of electromagnetic fields (EMF) on various sys­tems of the human body and animals with tumors, as well as on pain in the experiment and the clinic. The theoretical foundations and practical results of the use of EMF in various modulations and modes in the goals and objectives of oncology, including how to optimize the process of anesthesia and correct the vital activity of the body's functional systems with a tumor, are consecrated. Information is given on possible physicochemical effects, features, and mecha­nisms of therapeutic influence at various levels of a living organism. The ability of electromagnetic waves to transfer in­formation both within a single biosystem and at the level of a whole living organism with a tumor is shown. Studies of combined action of EMF and chemotherapy were analyzed. It has been established that there are experimental prerequisites for using this factor in order to induce changes in the permeability of the membranes of tumor cells by in­creasing the internalization of chemotherapeutic agents and, thus, enhance the antitumor effect. The role of EMF in the induction of apoptosis in tumor cells is shown. It has been shown that chemotherapy together with electromagnetic fields induces apoptosis and has an inhibitory effect on DNA synthesis in osteosarcoma cells, breast cancer, colon cancer, melanoma and other tumors. The role of magnetic fields in order to enhance the analgesic effect was investigated. The analgesic effect is due to the cessation or weakening of nerve impulses from the painful focus due to the elimination of hypoxia, the improvement of microcirculation, and the reduction of edema, it has been shown. Transcranial magnetic therapy is used as an analgesic tool in onconurology. The therapeutic anti-pain effect is associated with the stimulation of the antinociceptive system, an increase in the synthesis of natural analgesics — endorphins with their subsequent release into the cerebrospinal fluid and blood. As it has already been shown, with the increase in the intensity of pain and its duration, all indicators of the quality of life and the results of treatment of the patient deteriorate, so the search for ways to improve the antitumor effectiveness of specialized treatment and eliminate the causes that prevent their im­plementation continue to be relevant and in demand.

scholarly journals Mucin-1 (MUC1) as a promising molecular target in anticancer therapy

2019 ◽  
Vol 73 ◽  
pp. 53-64
Author(s):  
Agnieszka Gornowicz ◽  
Anna Bielawska ◽  
Bożena Popławska ◽  
Krzysztof Bielawski
Keyword(s):  
Tumor Cells ◽  
Anticancer Agents ◽  
Intracellular Signaling ◽  
Current Knowledge ◽  
P53 Protein ◽  
Chemotherapeutic Agents ◽  
Therapeutic Effects ◽  
Mucin 1 ◽  
Shock Proteins

Mucin 1 (MUC1) has been recognized by the National Cancer Institute as one of the most promising molecular targets in cancer therapy. Its overexpression has been demonstrated in many epithelial tumors,especially in breast cancer, whichis associated with poor prognosis. Mucin 1 is an important barrier to the penetration of drugs and takes part in the inhibition of apoptosis in tumor cells. MUC1 triggers the activation of several pathways of intracellular signaling. MUC1 interactions with ICAM-1, E-selectin, galectin-3, EGFR, ERα estrogen receptor, p53 protein, heat shock proteins HSP70 and HSP90 have been demonstrated. The MUC1 membrane subunit contributes to the activation of the ERK1 and ERK2 kinases by the induction of the Ras-Raf-Mek-Erk pathway. In addition, the role of MUC1 in the activation of the WNT/β-catenin/TCF7L2 pathway and the induction of transcription of the cyclin D1 gene was confirmed. Numerous studies have shown that blockade of MUC1 by monoclonal antibodies or small molecule inhibitors may promote therapeutic effects and contribute to increased susceptibility of tumor cells to chemotherapeutic agents. The combined effect of the anti-MUC1 antibody with novel anticancer agents may have a better therapeutic effect than monotherapy. This article reviews the current knowledge about the role of MUC1 in the development and progression of cancer as well as potential novel strategies based on mucin 1 in antineoplastic therapy.

scholarly journals Forskolin enhances the antitumor effect of oncolytic measles virus by promoting Rab27a dependent vesicular transport system in the lung cancer A549 cells in vitro

2020 ◽  
Author(s):  
Mao Xia ◽  
Yongquan Xia ◽  
Xuejing Xu ◽  
Gang Meng ◽  
Hong Yan ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Transport System ◽  
Measles Virus ◽  
Antitumor Effect ◽  
Vesicular Transport ◽  
A549 Cells ◽  
Over Expression ◽  
Combined Strategy

Abstract Background: Measles vaccine strain viruses (MV-Edm) are an ideal platform for developing safe and effective oncolytic vectors. However, despite the promising pre-clinical data, understanding of determinants of efficacy and, thus, the interplay of the oncolytic virus with particular agents remains limited.Methods: We investigated the potency of forskolin enhancing the antitumor effect of oncolytic measles virus by promoting Rab27a dependent vesicular transport system. Cells were infected with MV-Edm and the vesicles were observed by TEM. The oncolytic effects of MV-Edm/Forskolin were investigated in vitro. Results: Here we demonstrate that the MV-Edm infection and spread in tumor, which are indispensable processes for the viral oncolysis, depend on the vesicular transport system of tumor cells. On the contrary, the tumor cells display a responsive mechanism to restrain the MV-Edm spread by down-regulating the expression of Rab27a, which is a key member of the vesicle transport system. Over-expression of Rab27a promotes the oncolytic efficacy of MV-Edm towards A549 tumor cells. Finally, we find a Rab27a agonist Forskolin, is capable of promoting the oncolytic effect of MV-Edm in vitro. Conclusions: Our study reveals the important role of vesicle transporter Rab27a in the whole program of MV-Edm mediated oncolysis. We also provide a combined strategy of Forskolin and MV-Edm, which may exert a synergistic anti-tumor effect, for clinical treatment for patients with tumor.

scholarly journals Forskolin enhances the antitumor effect of oncolytic measles virus by promoting Rab27a dependent vesicular transport system

2020 ◽  
Author(s):  
Mao Xia ◽  
Yongquan Xia ◽  
Xuejing Xu ◽  
Gang Meng ◽  
Yan Hong ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Transport System ◽  
Measles Virus ◽  
Antitumor Effect ◽  
Vesicular Transport ◽  
Over Expression ◽  
Combined Strategy ◽  
Oncolytic Effect

Abstract Background Measles vaccine strain viruses (MV-Edm) are an ideal platform for developing safe and effective oncolytic vectors. However, despite the promising pre-clinical data, understanding of determinants of efficacy and, thus, the interplay of the oncolytic virus with particular agents remains limited. Methods We investigated the potency of forskolin enhancing the antitumor effect of oncolytic measles virus by promoting Rab27a dependent vesicular transport system. Cells were infected with MV-Edm and the vesicles were observed by TEM. The oncolytic effects of MV-Edm/Forskolin were investigated in vitro. Results Here we demonstrate that the MV-Edm infection and spread in tumor, which are indispensable processes for the viral oncolysis, depend on the vesicular transport system of tumor cells. On the contrary, the tumor cells display a responsive mechanism to restrain the MV-Edm spread by down-regulating the expression of Rab27a, which is a key member of the vesicle transport system. Over-expression of Rab27a promotes the oncolytic efficacy of MV-Edm towards A549 tumor cells. Finally, we find a Rab27a agonist Forskolin, is capable of promoting the oncolytic effect of MV-Edm in vitro. Conclusions Our study reveals the important role of vesicle transporter Rab27a in the whole program of MV-Edm mediated oncolysis. We also provide a combined strategy of Forskolin and MV-Edm, which may exert a synergistic anti-tumor effect, for clinical treatment for patients with tumor.

scholarly journals 5-Fluorouracil: A Narrative Review on the Role of Regulatory Mechanisms in Driving Resistance to This Chemotherapeutic Agent

2021 ◽  
Vol 11 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Atefe Abak ◽  
Farhad Tondro Anamag ◽  
Hamed Shoorei ◽  
Faranak Fattahi ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Epithelial Mesenchymal Transition ◽  
Chemotherapeutic Agent ◽  
Chemotherapeutic Agents ◽  
Regulatory Mechanisms ◽  
Cell Behavior ◽  
Mesenchymal Transition ◽  
Non Coding Rnas

5-fluorouracil (5-FU) is among the mostly administrated chemotherapeutic agents for a wide variety of neoplasms. Non-coding RNAs have a central impact on the determination of the response of patients to 5-FU. These transcripts via modulation of cancer-related pathways, cell apoptosis, autophagy, epithelial–mesenchymal transition, and other aspects of cell behavior can affect cell response to 5-FU. Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/β-catenin, Hedgehog, NF-kB, and Notch cascades. Moreover, there is an increasing interest in targeting these transcripts in various kinds of cancers that are treated by 5-FU. In the present article, we provide a review of the function of non-coding transcripts in the modulation of response of neoplastic cells to 5-FU.

scholarly journals miR-371b-5p-Engineered Exosomes Enhances Tumor Inhibitory Effect

2021 ◽  
Vol 9 ◽  
Author(s):  
Qiang Xue ◽  
Yang Yang ◽  
Linlin Yang ◽  
Xiaodi Yan ◽  
Zihao Shen ◽  
...  
Keyword(s):  
Cell Viability ◽  
Tumor Cells ◽  
Inhibitory Effect ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Drug Molecules ◽  
Tumor Tissues ◽  
Cellular Components

Background: Exosomes are well-known natural nanovesicles, that represent one of the recently discovered modes of intercellular communication due to their ability to transmit cellular components. Exosomes have been reported to have potential as natural vectors for carrying functional small RNAs and delivering chemotherapeutic agents to diseased cells. In this study, we aimed to investigate the role of exosomes in carrying miRNA for targeting tumor cells.Methods: We present a novel method for engineering exosomes with functional miR-317b-5b to target tumor cells. MiR-317b-5b exerts its anti-tumor function via its expression in tumors. RT-qPCR was performed to assess the levels of miR-371b-5p, FUT-4. Western blot was performed to measure the levels of CD9, CD81, and FUT-4 proteins. Confocal microscopy was used to observe the internalization of miR-317b-5b in tumor cells. CCK-8, EdU, flow cytometry, wound-healing migration and transwell assays were performed to evaluate cell viability, proliferation, migration, and invasion, respectively.Results: Our findings illustrated that miR-317b-5b-loaded engineered exosomes were internalized by tumor cells. MiR-317b-5b was overexpressed in tumor cells treated with miR-317b-5b-loaded engineered exosomes. The internalization of miR-317b-5b in tumor cells was accompanied by changes of cell viability, proliferation, apoptosis, and migratory and invasive capability. We found that miR-317b-5b-loaded engineered exosomes were presence in tumor tissue sections and miR-317b-5b was overexpressed in tumor tissues of osteosarcoma tumor-bearing mice infected with miR-317b-5b-loaded engineered exosomes. MiR-317b-5b-loaded engineered exosomes had the anti-tumor efficiency in vivo.Conclusion: Our findings show that miR-317b-5b-loaded engineered exosomes can be used as nanocarriers to deliver drug molecules such as miR-317b-5b both in vitro and in vivo to exert its anti-tumor functions.

scholarly journals Preparation of Targeted Platelet Carrier and Its Antitumor Effect

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 34-34
Author(s):  
Ying Du ◽  
Baoan Chen
Keyword(s):  
Tumor Cells ◽  
Antitumor Effect ◽  
Conflicts Of Interest ◽  
Drug Carrier ◽  
Myeloma Cell ◽  
Inhibitory Effect ◽  
Multiple Myeloma Cell ◽  
Human Multiple Myeloma

Objective:Tumor targeting proteins were modified on the surface of platelets and chemotherapeutic drugs were encapsulated in platelets. Based on the fact that platelets can enter the tumor environment and interact with tumor cells, the functionalized platelets carrier has dual targeting effect to kill tumor cells.Methods:Aspirin was used to inhibit platelets aggregation and deformation in vitro to obtain complete platelets. Exogenous Tf (transferrin) was modified on platelets surface to target specific tumor cells (human multiple myeloma cell line RPMI8226). DOX (doxorubicin) was loaded into platelets. To verify the inhibitory effect of functional platelets vector on cell. To observe the distribution of targeted functional platelets vector and treatment effect on implant tumor in mice.Results:Aspirin can inhibit platelets aggregation and deformation during the preparation process effectively. Stable platelets can be modified by Tf and encapsulate DOX effectively. At the same time, the functional platelet vector can specifically aggregate in the implant tumor site in vivo and achieve effective anti-tumor effect.Conclusion:Platelets aggregation and deformation can be inhibited by aspirin effectively, which makes it a stable natural drug carrier. The antitumor effect can be achieved by the functional platelets. Keywords:platelets, encapsulation, doxorubicin, tumor Disclosures No relevant conflicts of interest to declare.

scholarly journals Adjuvant Antitumor Immunity Contributes to the Overall Antitumor Effect of Pegylated Liposomal Doxorubicin (Doxil®) in C26 Tumor-Bearing Immunocompetent Mice

Pharmaceutics ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 990
Author(s):  
Takuma Takayama ◽  
Taro Shimizu ◽  
Amr S. Abu Lila ◽  
Yuki Kanazawa ◽  
Hidenori Ando ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tumor Cells ◽  
Antitumor Immunity ◽  
Antitumor Effect ◽  
Chemotherapeutic Agents ◽  
Therapeutic Effects ◽  
Cytotoxic Effects ◽  
Pegylated Liposomes ◽  
Immunocompetent Mice

Doxorubicin (DXR) has been reported to have direct cytotoxicity against cancer cells and indirect immunotoxicity by modulation of host antitumor immunity. Hence, it may prevent cancer progression by a dual mechanism. Doxil®, a formulation of DXR encapsulated in polyethylene glycol modified (PEGylated) liposomes, is the most widely used of the clinically approved liposomal anticancer drugs. However, the effect of Doxil® on host antitumor immunity is not well understood. In this study, Doxil® efficiently suppressed tumor growth in immunocompetent mice bearing C26 murine colorectal carcinomas, but not in T cell-deficient nude mice, indicating a contribution of T cells to the overall antitumor effect of Doxil®. In immunocompetent mice, Doxil® increased major histocompatibility complex (MHC-1) levels in C26 tumors, which may be an indicator of increased immunogenicity of tumor cells, and potentially amplified tumor immunogenicity by decreasing immunosuppressive cells such as regulatory T cells, tumor-associated microphages and myeloid-derived suppressor cells that collectively suppress T cell-mediated antitumor responses. This suggests that encapsulation of DXR into PEGylated liposomes increased the therapeutic efficacy of DXR though effects on host antitumor immunogenicity in addition to direct cytotoxic effects on tumor cells. This report describes the role of host antitumor immunity in the overall therapeutic effects of Doxil®. Manipulating pharmacokinetics and biodistribution of chemotherapeutic agents with immunomodulatory properties may increase their therapeutic efficacies by amplifying host antitumor immunity in addition to direct cytotoxic effects on tumor cells.

Activation of cytochrome c to a peroxidase compound I-type intermediate by H2O2: relevance to redox signalling in apoptosis

2004 ◽  
Vol 71 ◽  
pp. 97-106 ◽  
Author(s):  
Mark Burkitt ◽  
Clare Jones ◽  
Andrew Lawrence ◽  
Peter Wardman
Keyword(s):  
Cytochrome C ◽  
Hydroxyl Radical ◽  
Redox Regulation ◽  
Chemotherapeutic Agents ◽  
Tyrosyl Radical ◽  
Compound I ◽  
Definitive Evidence ◽  
Enhanced Production ◽  
Physico Chemical

The release of cytochrome c from mitochondria during apoptosis results in the enhanced production of superoxide radicals, which are converted to H2O2 by Mn-superoxide dismutase. We have been concerned with the role of cytochrome c/H2O2 in the induction of oxidative stress during apoptosis. Our initial studies showed that cytochrome c is a potent catalyst of 2′,7′-dichlorofluorescin oxidation, thereby explaining the increased rate of production of the fluorophore 2′,7′-dichlorofluorescein in apoptotic cells. Although it has been speculated that the oxidizing species may be a ferryl-haem intermediate, no definitive evidence for the formation of such a species has been reported. Alternatively, it is possible that the hydroxyl radical may be generated, as seen in the reaction of certain iron chelates with H2O2. By examining the effects of radical scavengers on 2′,7′-dichlorofluorescin oxidation by cytochrome c/H2O2, together with complementary EPR studies, we have demonstrated that the hydroxyl radical is not generated. Our findings point, instead, to the formation of a peroxidase compound I species, with one oxidizing equivalent present as an oxo-ferryl haem intermediate and the other as the tyrosyl radical identified by Barr and colleagues [Barr, Gunther, Deterding, Tomer and Mason (1996) J. Biol. Chem. 271, 15498-15503]. Studies with spin traps indicated that the oxo-ferryl haem is the active oxidant. These findings provide a physico-chemical basis for the redox changes that occur during apoptosis. Excessive changes (possibly catalysed by cytochrome c) may have implications for the redox regulation of cell death, including the sensitivity of tumour cells to chemotherapeutic agents.

The Role of the Interaction between Fe(III) and Cell Surface in the Accumulation of 67Ga by Tumor Cells

1991 ◽  
Vol 30 (06) ◽  
pp. 290-293 ◽  
Author(s):  
P. Maleki ◽  
A. Martinezi ◽  
M. C. Crone-Escanye ◽  
J. Robert ◽  
L. J. Anghileri
Keyword(s):  
Cell Surface ◽  
Tumor Cells ◽  
Ionic Composition ◽  
Iron Complex ◽  
Iron Binding ◽  
Complex Time ◽  
Interaction Product ◽  
Thermodynamic Constant ◽  
Number Of Cells

The study of the interaction between complexed iron and tumor cells in the presence of 67Ga-citrate indicates that a phenomenon of iron-binding related to the thermodynamic constant of stability of the iron complex, and a hydrolysis (or anion penetration) of the interaction product determine the uptake of 67Ga. The effects of various parameters such as ionic composition of the medium, nature of the iron complex, time of incubation and number of cells are discussed.

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

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