Sustainable approaches for the synthesis of biogenic platinum nanoparticles

Abstract Background The era of nanotechnology become widespread for research and human resource development due to its functionalized tuning with economical, eco-friendly, effective and sustainable end-products. Hence, the present review illustrates the biogenic fabrication of platinum nanoparticles (PtNPs) through the different sustainable and cheaper approaches. Main body of the abstract Over the physicochemical-based nanotechnology, the biogenic active substances-based synthesis displayed the more promising candidature due to its non-toxic, Broad-spectrum applicability and defendable type character. The biogenic synthesis method is capable with and without capping and highly motif of reducing agents. The morphology and stability of synthesized PtNPs are mostly mediated by various experimental conditions such as pH, temperature, incubation time, concentrations of biomaterials and salts or enzymes used. Hence, the review is aiming to discuss the methodology of biogenic synthesis of PtNPs by plant stem, root, leaf, flower, fruit, extracts, algae, fungi and egg yolk. Also, we have illustrated the pharmaceutical drug model application and its adverse effect. Short conclusion Synthesized PtNPs are open a new trend in catalyst, drug and its carrier and in cancer treatment. PtNPs are utilized as a new therapeutic agent for inhibiting the microbial pathogens with non-toxic behavior. The characterization of PtNPs could estimate the bio-sensitized properties which leads the commercial applications

Wilms' tumor protein induces an epithelial-mesenchymal hybrid differentiation state in clear cell renal cell carcinoma

The Wilms' tumor transcription factor (WT1) was originally classified as a tumor suppressor, but it is now known to also be associated with cancer progression and poor prognosis in several malignancies. WT1 plays an essential role in orchestrating a developmental process known as mesenchymal-to-epithelial transition (MET) during kidney development, but also induces the reverse process, epithelial-to-mesenchymal transition (EMT) during heart development. WT1 is not expressed in the adult kidney, but shows elevated expression in clear cell renal cell carcinoma (ccRCC). However, the role of WT1 in this disease has not been characterized. In this study, we demonstrate that WT1 is upregulated in ccRCC cells that are deficient in the expression of the von Hippel-Lindau tumor suppressor protein (VHL). We found that WT1 transcriptionally activated Snail, a master transcriptional repressor that is known to induce EMT. Although Snail represses E-cadherin and induces mesenchymal characteristics, we found partial maintenance of E-cadherin and associated epithelial characteristics in kidney cells and ccRCC cells that express WT1, since WT1 upregulates E-cadherin expression and competes with Snail repression. These findings support a novel paradigm in which WT1 induces an epithelial-mesenchymal hybrid transition (EMHT), characterized by Snail up-regulation with E-cadherin maintenance, a tumor cell differentiation state in which cancer cells keep both EMT and MET characteristics which may promote tumor cell plasticity and tumor progression.NIH grants P20GM103464 (Dr. Thomas Shaffer), DK56216 and the Nemours Foundation (A.K. Rajasekaran), SAF2010-16089 (A.G. de Herreros

WT1 regulates Snail expression.

<p>(A) Analysis of Snail protein (top) and mRNA (bottom) in the isogenic SN12C and ACHN cell lines. (B) HEK293T cells were transfected with scrambled oligonucleotides or VHL-specific siRNAs and Snail protein was measured. (C) HEK293T cells were transfected with GFP or GFP-WT1 and Snail protein (top) and mRNA (bottom) was measured. Graphs show mean±SD of one representative of three independent experiments. *, <i>P</i><0.05. (D) HEK293T and SN12C-VHL cells were transfected as indicated and protein expression was assessed by immunoblot.</p

WT1 upregulates E-cadherin expression in the presences of Snail.

<p>(A) Immunoblot analysis of E-cadherin and N-cadherin expression in the isogenic SN12C and ACHN cell lines. (B) VHL-knockdown RCC cells were transfected with scrambled or WT1-specifc siRNAs and E-cadherin expression was assessed by immunoblot. (C) Top, HEK293T cells were transfected as indicated and protein expression was assessed by immunoblot. Bottom, analysis of E-cadherin mRNA levels. (D, E) HEK293T (D) or MDCK (E) cells were cotransfected with the indicated plasmids and the <i>CDH1</i> promoter reporter construct, and luciferase activity was measured. Graphs represent mean±SD of one representative experiment. *, <i>P</i><0.05.</p

VHL-knockdown alters the expression of EMT markers in RCC cells.

<p>Representative phase-contrast and immunofluorescence images of the isogenic SN12C and ACHN cells. Scale bars = 100 µm in the phase-contrast images. Scale bars = 7.5 µm and 10 µm in the immunofluorescence images of the SN12C and ACHN cells, respectively.</p

WT1 transcriptionally upregulates Snail in VHL-deficient cells.

<p>(A) ChIP assays for WT1 were performed in the isogenic SN12C and ACHN cell lines. WT1 was immunoprecipitated and the bound DNA fragments were analyzed by PCR amplification for Snail. Histone H3 and rabbit IgG were used as positive and negative controls, respectively. Human RPL30 exon3 primers amplified a 160 bp fragment from immunoprecipitation of H3. Snail primers amplified a 120 bp fragment from immunoprecipitation using WT1 antibody. (B) <i>SNAI1</i> promoter luciferase activity was measured in the isogenic SN12C and ACHN cells. (C) SN12C-VHL and ACHN-VHL cells were cotransfected with either scrambled or siRNA-WT1 oligonucleotides, and <i>SNAI1</i> promoter luciferase activity was measured. Graphs depict mean±SD of one representative of three independent experiments. (D) Top, schematic representation of WT1 binding sequence within the Snail promoter with mutated residues highlighted with asterisks (***). Bottom, HEK293T cells were cotransfected with GFP or GFP-WT1 and either wild-type or mutated <i>SNAI1</i> promoter constructs and luciferase activity was measured. Graph depicts mean±SD of three independent experiments. *, <i>P</i><0.05.</p

WT1 preserves epithelial junctions and suppresses motility in renal cells.

<p>(A) MDCK cells were transfected as indicated and protein expression was assessed by immunoblot. (B) Representative immunofluorescene images of MDCK cells transfected with Snail alone or Snail and WT1. (C) Electron microscopy images of MDCK cells transfected with WT1, Snail, or WT1 and Snail. Red boxes indicate cell-cell contact regions showing intercellular junctions junctions enlarged in the inset (arrow). Note the absence of intercellular contacts and spindle morphology of Snail-transfected cells. (D) HEK293T cells were transfected with either GFP or GFP-WT1 and a scratch motility assay was performed. (E) Quantification of the width of the wound at the indicated time points. Graph depicts mean±SD of three independent experiments. *, <i>P</i><0.05.</p

Wilms' tumor protein induces an epithelial-mesenchymal hybrid differentiation state in clear cell renal cell carcinoma

The Wilms' tumor transcription factor (WT1) was originally classified as a tumor suppressor, but it is now known to also be associated with cancer progression and poor prognosis in several malignancies. WT1 plays an essential role in orchestrating a developmental process known as mesenchymal-to-epithelial transition (MET) during kidney development, but also induces the reverse process, epithelial-to-mesenchymal transition (EMT) during heart development. WT1 is not expressed in the adult kidney, but shows elevated expression in clear cell renal cell carcinoma (ccRCC). However, the role of WT1 in this disease has not been characterized. In this study, we demonstrate that WT1 is upregulated in ccRCC cells that are deficient in the expression of the von Hippel-Lindau tumor suppressor protein (VHL). We found that WT1 transcriptionally activated Snail, a master transcriptional repressor that is known to induce EMT. Although Snail represses E-cadherin and induces mesenchymal characteristics, we found partial maintenance of E-cadherin and associated epithelial characteristics in kidney cells and ccRCC cells that express WT1, since WT1 upregulates E-cadherin expression and competes with Snail repression. These findings support a novel paradigm in which WT1 induces an epithelial-mesenchymal hybrid transition (EMHT), characterized by Snail up-regulation with E-cadherin maintenance, a tumor cell differentiation state in which cancer cells keep both EMT and MET characteristics which may promote tumor cell plasticity and tumor progression.NIH grants P20GM103464 (Dr. Thomas Shaffer), DK56216 and the Nemours Foundation (A.K. Rajasekaran), SAF2010-16089 (A.G. de Herreros