Inhibitory effect of Par-4 combined with cisplatin on human Wilms’ tumor cells

Natural killer (NK) cells play a key role in the control of cancer development, progression and metastatic dissemination. However, tumor cells develop an array of strategies capable of impairing the activation and function of the immune system, including NK cells. In this context, a major event is represented by the establishment of an immunosuppressive tumor microenvironment (TME) composed of stromal cells, myeloid-derived suppressor cells, tumor-associated macrophages, regulatory T cells and cancer cells themselves. The different immunoregulatory cells infiltrating the TME, through the release of several immunosuppressive molecules or by cell-to-cell interactions, cause an impairment of the recruitment of NK cells and other lymphocytes with effector functions. The different mechanisms by which stromal and tumor cells impair NK cell function have been particularly explored in adult solid tumors and, in less depth, investigated and discussed in a pediatric setting. In this review, we will compare pediatric and adult solid malignancies concerning the respective mechanisms of NK cell inhibition, highlighting novel key data in neuroblastoma and Wilms’ tumor, two of the most frequent pediatric extracranial solid tumors. Indeed, both tumors are characterized by the presence of stromal cells acting through the release of immunosuppressive molecules. In addition, specific tumor cell subsets inhibit NK cell cytotoxic function by cell-to-cell contact mechanisms likely controlled by the transcriptional coactivator TAZ. These findings could lead to a more performant diagnostic approach and to the development of novel immunotherapeutic strategies targeting the identified cellular and molecular targets.

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566: Comparative Genomic Hybridization of Chemotherapy Survived Wilms' Tumor Cells

The Journal of Urology ◽

10.1016/s0022-5347(18)37828-5 ◽

2004 ◽

Vol 171 (4S) ◽

pp. 150-151

Author(s):

Thorsten Schlomm ◽

Bastian Gunawan ◽

Hans J. Schulten ◽

Norbert Graf ◽

Ivo Leuschner ◽

...

Keyword(s):

Tumor Cells ◽

Comparative Genomic Hybridization ◽

Wilms Tumor ◽

Comparative Genomic ◽

Genomic Hybridization

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RGD4C peptide mediates anti-p21Ras scFv entry into tumor cells and produces an inhibitory effect on the human colon cancer cell line SW480

BMC Cancer ◽

10.1186/s12885-021-08056-4 ◽

2021 ◽

Vol 21 (1) ◽

Cited By ~ 1

Author(s):

Chen-Chen Huang ◽

Fang-Rui Liu ◽

Qiang Feng ◽

Xin-Yan Pan ◽

Shu-Ling Song ◽

...

Keyword(s):

Antitumor Activity ◽

Cell Membrane ◽

Fusion Protein ◽

Tumor Cell ◽

Tumor Cells ◽

Fusion Proteins ◽

Inhibitory Effect ◽

Endosomal Escape ◽

Antitumor Effects ◽

Sw480 Cells

Abstract Background We prepared an anti-p21Ras scFv which could specifically bind with mutant and wild-type p21Ras. However, it cannot penetrate the cell membrane, which prevents it from binding to p21Ras in the cytoplasm. Here, the RGD4C peptide was used to mediate the scFv penetration into tumor cells and produce antitumor effects. Methods RGD4C-EGFP and RGD4C-p21Ras-scFv recombinant expression plasmids were constructed to express fusion proteins in E. coli, then the fusion proteins were purified with HisPur Ni-NTA. RGD4C-EGFP was used as reporter to test the factors affecting RGD4C penetration into tumor cell. The immunoreactivity of RGD4C-p21Ras-scFv toward p21Ras was identified by ELISA and western blotting. The ability of RGD4C-p21Ras-scFv to penetrate SW480 cells and colocalization with Ras protein was detected by immunocytochemistry and immunofluorescence. The antitumor activity of the RGD4C-p21Ras-scFv was assessed with the MTT, TUNEL, colony formation and cell migration assays. Chloroquine (CQ) was used an endosomal escape enhancing agent to enhance endosomal escape of RGD4C-scFv. Results RGD4C-p21Ras-scFv fusion protein were successfully expressed and purified. We found that the RGD4C fusion protein could penetrate into tumor cells, but the tumor cell entry of was time and concentration dependent. Endocytosis inhibitors and a low temperature inhibited RGD4C fusion protein endocytosis into cells. The change of the cell membrane potential did not affect penetrability. RGD4C-p21Ras-scFv could penetrate SW480 cells, effectively inhibit the growth, proliferation and migration of SW480 cells and promote this cells apoptosis. In addition, chloroquine (CQ) could increase endosomal escape and improve antitumor activity of RGD4C-scFv in SW480 cells. Conclusion The RGD4C peptide can mediate anti-p21Ras scFv entry into SW480 cells and produce an inhibitory effect, which indicates that RGD4C-p21Ras-scFv may be a potential therapeutic antibody for the treatment of ras-driven cancers.

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Loss of allelic heterozygosity at a second locus on chromosome 11 in sporadic Wilms' tumor cells.

Molecular and Cellular Biology ◽

10.1128/mcb.9.4.1799 ◽

1989 ◽

Vol 9 (4) ◽

pp. 1799-1803 ◽

Cited By ~ 145

Author(s):

A E Reeve ◽

S A Sih ◽

A M Raizis ◽

A P Feinberg

Keyword(s):

Mental Retardation ◽

Tumor Cells ◽

Germ Line ◽

Wilms Tumor ◽

Globin Gene ◽

Allelic Loss ◽

Chromosomal Band ◽

Chromosome 11 ◽

Gamma Globin ◽

Wagr Syndrome

Children with associated Wilms' tumor, aniridia, genitourinary malformations, and mental retardation (WAGR syndrome) frequently have a cytogenetically visible germ line deletion of chromosomal band 11p13. In accordance with the Knudson hypothesis of two-hit carcinogenesis, the absence of this chromosomal band suggests that loss of both alleles of a gene at 11p13 causes Wilms' tumor. Consistent with this model, chromosomes from sporadically occurring Wilms' tumor cells frequently show loss of allelic heterozygosity at polymorphic 11p15 loci, and therefore it has been assumed that allelic loss extends proximally to include 11p13. We report here that in samples from five sporadic Wilms' tumors, allelic loss occurred distal to the WAGR locus on 11p13. In cells from one tumor, mitotic recombination occurred distal to the gamma-globin gene on 11p15.5. Thus, allelic loss in sporadic Wilms' tumor cells may involve a second locus on 11p.

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KDM6B Inhibition Has Anti-Tumor Activity in Anaplastic Wilms Tumor Cells Associated with WT1 And MYCN Pathway Silencing

10.1542/peds.147.3_meetingabstract.914-a ◽

2021 ◽

Author(s):

Hyea Jin Gil ◽

Emilia M. Pinto ◽

Andrew M. Davidoff ◽

Gerard P. Zambetti ◽

Jun Yang ◽

...

Keyword(s):

Tumor Cells ◽

Wilms Tumor ◽

Anti Tumor Activity

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Action inhibitrice des cellules irradiées sur la greffe des cellules actives dans la tumeur T8 de Guérin. (Inhibitory effect of irradiated tumor cells of Guérin T8 tumor on the growth of viable cells)

Plastic & Reconstructive Surgery ◽

10.1097/00006534-196204000-00055 ◽

1962 ◽

Vol 29 (4) ◽

pp. 489

Author(s):

&NA;

Keyword(s):

Tumor Cells ◽

Inhibitory Effect ◽

Viable Cells

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MicroRNA-27a-5p inhibits proliferation, migration and invasion and promotes apoptosis of Wilms tumor cell by targeting PBOV1

10.1101/2021.08.25.457737 ◽

2021 ◽

Author(s):

zhengtuan guo ◽

qiang yv ◽

chunlin miao ◽

wenan ge ◽

peng li

Keyword(s):

Tumor Cells ◽

Wilms Tumor ◽

Suppressive Effect ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Tumor Tissues ◽

And Function ◽

Tumor Suppressive Effect

Wilms tumor is the most common type of renal tumor in children. MicroRNAs (miRNA) are small non-coding RNAs that play crucial regulatory roles in tumorigenesis. We aimed to study the expression profile and function of miR-27a-5p in Wilms tumor. MiR-27a-5p expression was downregulated in human Wilms tumor tissues. Functionally, overexpression of miR-27a-5p promoted cell apoptosis of Wilms tumor cells. Furthermore, upregulated miR-27a-5p delayed xenograft Wilms tumor tumorigenesis in vivo. Bioinformatics analysis predicted miR-27-5p directly targeted to the 3’-untranslated region (UTR) of PBOV1 and luciferase reporter assay confirmed the interaction between miR-27a-5p and PBOV1. The function of PBOV1 in Wilms tumor was evaluated in vitro and knockdown of PBOV1 dampened cell migration. In addition, overexpression of PBOV1 antagonized the tumor-suppressive effect of miR-27a-5p in Wilms tumor cells. Collectively, our findings reveal the regulatory axis of miR-27-5p/PBOV1 in Wilms tumor and miR-27a-5p might serve as a novel therapeutic target in Wilms tumor.

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

Research n Practical Medicine Journal ◽

10.17709/2409-2231-2019-6-2-9 ◽

2019 ◽

Vol 6 (2) ◽

pp. 86-99 ◽

Cited By ~ 2

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.

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