Time-resolved photoluminescence study of CdSe/CdMnS/CdS core/multi-shell nanoplatelets

We used photoluminescence spectroscopy to resolve two emission features in CdSe/CdMnS/CdS and CdSe/CdS core/multi-shell nanoplatelet heterostructures. The photoluminescence from the magnetic sample has a positive circular polarization with a maximum centered at the position of the lower energy feature. The higher energy feature has a corresponding signature in the absorption spectrum; this is not the case for the low-energy feature. We have also studied the temporal evolution of these features using a pulsed-excitation/time-resolved photoluminescence technique to investigate their corresponding recombination channels. A model was used to analyze the temporal dynamics of the photoluminescence which yielded two distinct timescales associated with these recombination channels. The above results indicate that the low-energy feature is associated with recombination of electrons with holes localized at the core/shell interfaces; the high-energy feature, on the other hand, is excitonic in nature with the holes confined within the CdSe cores. © 2016 Author(s)

Time resolved photoluminescence study of magnetic CdSe/CdMnS/CdS core/multi-shell nanoplatelets

Colloidal semiconductor nanoplatelets (NPLs) are quasi 2D-nanostructures that are grown and processed inexpensively using a solution based method and thus have recently attracted considerable attention. We observe two features in the photoluminescence spectrum, suggesting two possible recombination channels. Their intensity ratio varies with temperature and two distinct temperature regions are identified; a low temperature region (10K < T < 90K) and a high temperature region (90K < T < 200K). This ratio increases with increasing temperature, suggesting that one recombination channel involves holes that are weakly localized with a localization energy of 0.043meV. A possible origin of these localized states are energy-variations in the xy-plane of the nanoplatelet. The presence of positive photoluminescence circular polarization in the magnetically-doped core/multi-shell NPLs indicates a hole-dopant exchange interaction and therefore the incorporated magnetic Manganese ions act as a marker that determines the location of the localized hole states.1 Time-resolved measurements show two distinct timescales (τfast and τslow) that can be modeled using a rate equation model. We identify these timescales as closely related to the corresponding recombination times for the channels. The stronger hole localization of one of these channels leads to a decreased electron-hole wave function overlap and thus a decreased oscillator strength and an increased lifetime. We show that we can model and understand the magnetic interaction of doped 2D-colloidal nanoplatelets which opens a pathway to solution processable spin controllable light sources. Copyright © 2017 SPIE

Magneto-optical studies of CdSe/CdMnS/CdS core/multi-shell colloidal nanoplatelets

We studied the photoluminescence (PL)) from CdSe/CdMnS/CdS core/multi-shell colloidal nanoplatelets, a versatile platform to study the interplay of optical properties and nanomagnetism. The photoluminescence (PL) exhibits σ+ polarization in the applied magnetic field. Our measurement detects the presence of even a single magnetic monolayer shell. The PLL consists of a higher and a lower energy component; the latter exhibits a circular polarization peak. The time-resolved PL (trPL) shows a red shift as function of time delay. At early (later) times the trPL spectra coincide with the high (low) energy PL component. A model is proposed to interpret these results. © 2016 SPIE

The Tumor Suppressor Gene, RASSF1A, Is Essential for Protection against Inflammation -Induced Injury

10.1371/journal.pone.0075483PLoS ONE810-POLN

Use of the xCELLigence system for real-time analysis of changes in cellular motility and adhesion in physiological conditions.

Investigation of the mechanisms behind the regulation of cellular motility and adhesion is key to understanding metastasis and the biology of tumor spreading. There are many technologies available for these studies, but the majority of them are either dependent on the use of labels or limited to endpoint analysis. The xCELLigence RTCA (real-time cell analysis) provides a platform for label free and operator independent investigation of the migration, invasion and adhesion proprieties of cells in physiologically relevant conditions. The real-time kinetic data acquisition also allows for a more accurate characterization of short-lived cellular events. In this chapter we describe the use of the xCELLigence Real-Time Cell Analyzer to investigate changes in cellular adhesion and motility in real time

ATM regulates a RASSF1A-dependent DNA damage response.

Hypermethylation of CpG islands in the RASSF1 promoter is one of the most frequent events identified in human cancer. The epigenetic-driven loss of RASSF1A protein expression is observed more often in tumors of higher grade and correlates with a decreased responsiveness to DNA-damaging therapy. Ras association domain-containing family 1A (RASSF1A) promotes apoptosis by signaling through the MST2 and LATS1 kinases, leading to stabilization of the YAP1/p73 transcriptional complex. Here we provide evidence for a new pathway linking DNA damage signaling to RASSF1A via the main sensor of double-strand breaks in cells, ataxia telangiectasia mutated (ATM). We show that, upon DNA damage, RASSF1A is phosphorylated by ATM on Ser131 and is involved in the activation of both MST2 and LATS1, leading to the stabilization of p73. Furthermore, lung and ovarian tumor cell lines that retain RASSF1A expression commonly harbor polymorphisms in the region of Ser131, and our analysis shows that the S131F polymorphism conveys resistance to DNA-damaging agents. Thus, we present a novel DNA damage pathway emanating from ATM that is frequently disabled in tumors via epigenetic silencing of RASSF1 or mutation of an ATM phosphorylation site

TGF-β targets the hippo pathway scaffold RASSF1A to facilitate YAP/SMAD2 nuclear translocation

Epigenetic inactivation of the Hippo pathway scaffold RASSF1A is associated with poor prognosis in a wide range of sporadic human cancers. Loss of expression reduces tumor suppressor activity and promotes genomic instability, but how this pleiotropic biomarker is regulated at the protein level is unknown. Here we show that TGF-β is the physiological signal that stimulates RASSF1A degradation by the ubiquitin-proteasome pathway. In response to TGF-β, RASSF1A is recruited to TGF-β receptor I and targeted for degradation by the co-recruited E3 ubiquitin ligase ITCH. RASSF1A degradation is necessary to permit Hippo pathway effector YAP1 association with SMADs and subsequent nuclear translocation of receptor-activated SMAD2. We find that RASSF1A expression regulates TGF-β-induced YAP1/SMAD2 interaction and leads to SMAD2 cytoplasmic retention and inefficient transcription of TGF-β targets genes. Moreover, RASSF1A limits TGF-β induced invasion, offering a new framework on how RASSF1A affects YAP1 transcriptional output and elicits its tumor-suppressive function

RASSF1C oncogene elicits amoeboid invasion, cancer stemness, and extracellular vesicle release via a SRC/Rho axis

Cell plasticity is a crucial hallmark leading to cancer metastasis. Upregulation of Rho/ROCK pathway drives actomyosin contractility, protrusive forces, and contributes to the occurrence of highly invasive amoeboid cells in tumors. Cancer stem cells are similarly associated with metastasis, but how these populations arise in tumors is not fully understood. Here, we show that the novel oncogene RASSF1C drives mesenchymal-to-amoeboid transition and stem cell attributes in breast cancer cells. Mechanistically, RASSF1C activates Rho/ROCK via SRC-mediated RhoGDI inhibition, resulting in generation of actomyosin contractility. Moreover, we demonstrate that RASSF1C-induced amoeboid cells display increased expression of cancer stem-like markers such as CD133, ALDH1, and Nanog, and are accompanied by higher invasive potential in vitro and in vivo. Further, RASSF1C-induced amoeboid cells employ extracellular vesicles to transfer the invasive phenotype to target cells and tissue. Importantly, the underlying RASSF1C-driven biological processes concur to explain clinical data: namely, methylation of the RASSF1C promoter correlates with better survival in early-stage breast cancer patients. Therefore, we propose the use of RASSF1 gene promoter methylation status as a biomarker for patient stratification