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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 73 records · Page 4
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Lycorine possesses notable anticancer potentials in on-small cell lung carcinoma cells via blocking Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT)

Highlights: • As a natural active alkaloid, the molecular mechanism of lycorine for NSCLC is still unclear. • Lycorine induced NSCLC to apoptosis at early-period apoptosis. • Lycorine suppressed Wnt/β-catenin signaling and reversed EMT. • Lycorine inhibition of the proliferation and metastasis of NSCLC in A549/Luc xenograft model. • Results provided a novel evidence for lycorine as natural anticaner agents to combat NSCLC. Lycorine, an natural isoquinoline alkaloid has reportedly that possesses multi-anticancer activity. However, to date, the anticancer feature of lycorine in non-small cell lung carcinoma (NSCLC) has still not fully been spelled out. The present study mainly focused on the molecular mechanism of lycorine against NSCLC in vitro and vivo. The results showed that lycorine evidently inhibited proliferation of A549 and H460 with IC{sub 50} values were 10.83 ± 1.14 μM and 12.35 ± 1.13 μM, while caused slight cytotoxicity in normal pulmonary epithelial Beas-2B cells, and arrested cell cycle in G0/G1 phase. Hoechst DNA-binding staining showed that typical characteristics of nuclear morphology apoptosis, AnnexinV-FITC/PI staining revealed the early-period apoptosis and the dissipation of mitochondrial membrane potential (Δψm) were also captured after lycorine treatment. Moreover, lycorine effectively repressed the Wnt/β-catenin signaling and reversed epithelial-mesenchymal transition (EMT). In addition, lycorine also intervened the caspase-mediated mitochondrial apoptosis pathway. Furthermore, A549/Luc tumor xenograft model was also corroborated that lycorine significantly suppressed the growth and metastasis of the lung tumor. These data highlight the significance of lycorine as potential anti-neoplastic agents to combat NSCLC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

LncRNA TP73-AS1 predicts the prognosis of bladder cancer patients and functions as a suppressor for bladder cancer by EMT pathway

Highlights: • LncRNA TP73-AS1 is identified with downregulation in bladder cancer tissues and cell lines. • Patients with low TP73-AS1 have shorter overall survival and progression-free survival. • Overexpression of TP73-AS1 can inhibit cell growth, migration, and invasion in vitro study. • Overexpression of TP73-AS1 inhibits metastasis of bladder cancer cell through inactivating EMT pathway. • We firstly reported the tumor suppressor function of TP73-AS1 in bladder cancer. Long noncoding RNAs (lncRNAs) have been identified to have more and more important roles in tumorigenesis and may be novel biomarker for cancer therapy. LncRNA TP73-AS1 is a novel identified lncRNA that has been demonstrated to be increased in several cancers, however, its function in bladder cancer remains unknown. The aim of this work was to examine the expression and role of lncRNA TP73-AS1 in bladder cancer. The expression levels of lncRNA TP73-AS1 in bladder cancer tissues and cell lines were determined by quantitative real-time PCR (qRT-PCR), and its clinical significance was assessed by statistical analysis. Moreover, by gain-of-function assay, the effect of TP73-AS1 on proliferation, cell cycle, apoptosis, migration and invasion was examined in bladder cancer cells. We identified that the expression level of TP73-AS1 was significantly down-regulated in bladder cancer tissues and cells compared to adjacent non-tumor tissues. Kaplan-Meier survival analysis found that patients with low TP73-AS1 expression level had shorter overall survival and progression-free survival than those with high TP73-AS1 expression. Moreover, we showed that overexpression of TP73-AS1 could inhibit cell growth, arrest cell cycle, reduce cell migration and invasion, and promote cell apotosis in vitro study. In addition, overexpression of TP73-AS1 diminished epithelial-mesenchymal transition (EMT) through inhibiting the expression of vimentin, snail, MMP-2, and MMP-9 and upregulating the expression levels of E-cadherin. Collectively, our findings for the first time elucidated that lncRNA TP73-AS1 may serve as a tumor suppressor participated in bladder cancer progression, which provided a promising therapy strategy for patients with bladder cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

USP10 regulates the stability of the EMT-transcription factor Slug/SNAI2

Highlights: • By undertaking a genome-wide siRNA screen, we have identified USP10 as regulator of Slug stability. • We show that USP10 binds Slug and mediates its degradation by the proteasome. • We provide detailed evidences that genetic depletion of USP10 causes beyond, a reduction of Slug, also suppress Vimetin levels (a hallmark mesenchymal marker) and migration. • Reversely, expression of USP10 stabilizes and elevates Slug. • Importantly, we show that USP10 expression correlates with Slug expression in primary tumor biopsies. Epithelial-to-mesenchymal transition (EMT) is a fundamental mechanism governing the switch of cells from an epithelial to a motile mesenchymal-like state. This transdifferentiation is regulated by key transcription factors, including Slug. The stability and function of Slug can be regulated by multiple mechanisms, including ubiquitin-mediated post-translational modifications. Here, by using a genome wide siRNA screen for human deubiquitinating enzymes (DUBs), we identified USP10 as a deubiquitinase for Slug in cancer cells. USP10 interacts with Slug and mediates its degradation by the proteasome. Importantly, USP10 is concomitantly highly expressed with Slug in cancer biopsies. Genetic knockdown of USP10 leads to suppressed Slug levels with a decreased expression of the mesenchymal marker Vimentin. Further, it reduces the migratory capacity of cancer cells. Reversely, overexpression of USP10 elevates the level of both Slug and Vimentin. Our study identifies USP10 as a regulator of the EMT-transcription factor Slug and cell migration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

AURKA contributes to the progression of oral squamous cell carcinoma (OSCC) through modulating epithelial-to-mesenchymal transition (EMT) and apoptosis via the regulation of ROS

Highlights: • AURKA knockdown inhibited the proliferation and ETM in OSCC cell lines. • Silencing AURKA induced apoptosis and ROS in OSCC cell lines. • AURKA knockdown inhibited tumor growth in vivo. Oral squamous cell carcinoma (OSCC) is known as one of the most common cancer influencing the head and neck region. However, the molecular mechanisms revealing OSCC progression is largely unclear. Aurora kinase A (AURKA) is a serine-threonine kinase that functions in mitotic spindle formation and chromosome segregation, and is associated with the progression of human cancers. But its role in regulating OSCC development has not yet been investigated. In the study, we found that AURKA expression was up-regulated in OSCC cell lines and tumor specimens from patients. OSCC patients with high expression of AURKA exhibited a significant decreased overall survival rate. In vitro, AURKA knockdown markedly reduced the proliferation, migration and invasion of OSCC cells using cell counting kit-8 (CCK-8), EdU, colony formation and transwell analysis. EMT was suppressed by AURKA silence, as evidenced by the up-regulated expression of E-cadherin and down-regulated Vimentin in OSCC cells. In addition, apoptosis was markedly induced by AURKA inhibition through promoting the expression of cleaved Caspase-3 and poly (ADP)-ribose polymerase (PARP). Reactive oxygen species (ROS) production was also markedly enhanced in AURKA-knockdown OSCC cells. Importantly, we found that repressing ROS generation using its scavenger of n-acetylcysteine (NAC) significantly abolished AURKA silence-induced apoptosis, accompanied with restored proliferation and EMT. In vivo, AURKA knockdown notably inhibited tumor growth. Therefore, knockdown of AURKA suppressed cell proliferation, migration and invasion, and also induced apoptosis and ROS generation in OSCC possibly via the production of ROS, demonstrating that AURKA inhibition might represent a novel therapeutic target for the prevention of OSCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Tiam1 promotes thyroid carcinoma metastasis by modulating EMT via Wnt/β-catenin signaling

Aberrant expression of the guanine nucleotide exchange factor Tiam1 is implicated in the invasive phenotype of many cancers. However, its involvement in thyroid carcinoma and downstream molecular events remains largely undefined. Here, we examined the effects of Tiam1 on the invasiveness and metastasis of thyroid carcinoma in vitro and in vivo and explored the underlying mechanisms by investigating the regulation of Tiam1 expression and the downstream pathways affected. Our results showed that Tiam1 knockdown inhibited the migratory and invasive capacity of thyroid cancer cells, suppressed epithelial-mesenchymal transition (EMT), and inhibited Wnt/β-catenin signaling in vitro. Moreover, Tiam1 knockdown suppressed liver metastasis development in vivo. The effects of Tiam1 on metastasis and EMT mediated by the Wnt/β-catenin pathway were reversed by Rac1 silencing, suggesting that the prometastatic effect of Tiam1 is mediated by the activation of Rac1. These results indicate that Tiam1 may be a prognostic factor and potential therapeutic target for the treatment of thyroid cancers.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

TWIST2 inhibits EMT and induces oxidative stress in lung cancer cells by regulating the FGF21-mediated AMPK/mTOR pathway

Twist related protein 2 (TWIST2) plays an important role in bone development, tumorigenesis, tumour progression and epithelial mesenchymal transition (EMT). At present, there are few reports about the role of TWIST2 in lung cancer, which need to be further explored. Therefore, the purpose of this study is to explore the role and molecular mechanism of TWIST2 in the occurrence and development of lung cancer. The expression of TWIST2 in tissues of patients and cell lines was measured using RT-qPCR and western blotting. MTT and CCK8 assays were used to detect cell proliferation and viability. Western blotting was used to measure the expression of EMT-related proteins, including E-cadherin, N-cadherin, Vimentin and Slug. The results revealed that TWIST2 is lowly expressed in the tissues of lung cancer patients and cell lines. Further studies found that overexpression of TWIST2 significantly induced apoptosis and promoted the expression of E-cadherin, as well as inhibiting the expression of N-cadherin, Vimentin and Slug. More importantly, TWIST2 induced oxidative stress in lung cancer cells. In addition, TWIST2 regulated the FGF21 and AMPK/mTOR signalling pathway, which is involved in the molecular mechanism of the gene in lung cancer cells. We suggest that the mechanism of TWIST2 inhibition of the progression of lung cancer is by regulating the FGF21-mediated AMPK/mTOR signalling pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2024

Benchmark High-Fidelity EMT Models for Power Grid with PV Plants

In recent times electromagnetic transient (EMT) modeling tools have been identified as one of the most important requirements in replicating, analyzing, and investigating the dynamics of the power grid with photovoltaic (PV) plants. However, there are no benchmark models for power grid with PVs to investigate emerging challenges with higher penetration of PVs (like trips and momentary cessations during faults from a region far away). To this end, in this paper, synthetic benchmark high-fidelity EMT dynamic models of power grid with large-scale PV plants are presented. The models are developed in PSCAD and PSCAD/Fortran. Simulation results for different use cases (events) and scenarios are presented.

Marthi, Phani Ratna Vanamali↗
DOE OSTI2025

Control Design and EMT Simulation Toward the Restoration of Faulted Wind-Dominant Grids

Present power engineers have been challenged to employ electromagnetic transient (EMT) simulations to study the restoration of wind-dominant grids. This paper addresses this hurdle by developing strategies to: (i) reliably control the dc-link voltage of grid-forming wind turbines with dc-coupled batteries, (ii) tune controllers to stably interconnect wind power plants into a grid under recovery, and (iii) autonomously make restoration decisions if transmission faults occur during restoration. These contributions are assessed via EMT simulations of wind-dominant versions of the WSCC 9-bus grid and a 22-bus power system. Furthermore, this paper is significant to address recommendations by the North American Electric Reliability Corporation.

17 WIND ENERGY↗
DOE OSTI2025

Analysis of a Disturbance Event with Inverter-Based Resources Using EMT Simulations

Increasing penetration of inverter-based resources (IBRs) necessitates newer methods of planning and analysis of disturbances. The existing phasor-domain transient stability (TS) analysis may not capture the dynamics of IBRs during fault events. Here, in this paper, electromagnetic transient (EMT) simulations using high-fidelity detailed model of power grid and one of the affected photovoltaic (PV) plants during the Angeles Forest disturbance in 2018 are performed. In these simulations, the processes to develop EMT models of power grid from traditional phasor-domain TS data and PV plant from collected data are described. Thereafter, using these simulations, the response of the PV plant during the fault event in 2018 is replicated and a sensitivity analysis is performed. The sensitivity analysis consists of making changes to the components within the PV plant and in the power grid to evaluate the impact they have on the response observed by the PV plant during the fault event. This analysis provides an understanding of the components that impact the operation of a PV plant during fault events and provide guidance to system planners on the studies that need to be performed to maintain a reliable power grid as new IBR plants are integrated.

42 ENGINEERING↗
DOE OSTI2025

Intelligently Partitioned Phasor-EMT Hybrid Simulations of Large-Scale, High-IBR Power Systems

As the penetration level of power electronics-interfaced renewables such as photovoltaics (PV) and wind has surged in modern electric grids, new operational risks caused by the dynamics of those inverter-based resources (IBRs) are emerging in parallel. Lessons learned from various grid events include that the impact of IBRs on system-level grid stability will become prominent along with the increase of renewables and that the short-timescale dynamic impacts of IBRs on grid stability are not fully captured by current commercial dynamic simulation tools [1] [2]. For example, IBRs can be controlled to mitigate those destabilizing interactions, but conventional phasor-domain tools (e.g. PSS/E, PSLF) often cannot capture that; likewise, the existing electromagnetic transient (EMT) simulation tools (e.g. PSCAD, EMTP) can simulate detailed IBR controls, but for large power systems with many IBRs, slow simulation speeds severely impede the ability to study dynamic events [3] [4]. Massively paralleling simulations using high-performance computing (HPC) can help address this, especially now that cloud-based HPC capability is widely available, but today s EMT tools are not HPC-compatible, and parallelization of dynamic simulation solvers is not trivial because each region can dynamically affect the others. Thus, dynamic simulation of grids with very large numbers of IBRs potentially poses a barrier to the ongoing energy transition.

24 POWER TRANSMISSION AND DISTRIBUTION↗
DOE OSTI2018

Catalpol suppresses osteosarcoma cell proliferation through blocking epithelial-mesenchymal transition (EMT) and inducing apoptosis

Highlights: • Catalpol inhibits cell viability and EMT in osteosarcoma cell lines. • Catalpol induces apoptosis in osteosarcoma cell lines by Bcl-2/Caspase-8 signaling. • Catalpol induces ROS generation and suppresses STAT3 pathway activation. • Catalpol is able to suppresses osteosarcoma growth in vivo. Catalpol, an iridoid glucoside compound, is reported to possess diverse pharmacological actions. However, its effects on osteosarcoma are little to be known. In the present study, we showed that catalpol could strongly suppress osteosarcoma progression. Catalpol dose-dependently reduced the cancer cell viability. The migration of osteosarcoma cells was also consistently suppressed by catalpol treatment using the wound healing and transwell migration analysis. Catalpol reduced the expressions of Kras, receptor for activated C-kinase 1(RACK1) and matrix metalloproteinase (MMP)-2 in a dose-dependent manner, revealing the blockage of migration. Moreover, both intrinsic and extrinsic apoptosis were triggered by catalpol, as evidenced by improved cleaved Caspase-8/-9/-3 and Poly-(ADP-ribose) polymerase (PARP). Release of Cyto-c in cytoplasm and Bax up-regulation in total cells were observed in catalpol-treated cells, while mitochondrial Cyto-c and cellular Bcl-2 were down-regulated by catalpol. Reactive oxygen species (ROS) production was also involved in catalpol-induced cell death. Further, ROS scavenger, N-acetylcysteine (NAC), impeded catalpol-caused apoptosis. And suppression of signal transducer and activator of transcription 3/Janus kinase 2 gene/Src (STAT3/JAK2/Src) was involved in catalpol-induced cell death. In vivo, catalpol showed effective ability to reduce the tumor growth. Our results illustrated that catalpol might be considered as a promising pharmacological agent to suppress osteosarcoma.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Effects of saponins of patrinia villosa against invasion and metastasis in colorectal cancer cell through NF-κB signaling pathway and EMT

Research has indicated that Herba Patriniae can suppress the growth of Several kinds of tumor cells in vitro and in vivo, thus displaying favorable antitumor activity. However, research regarding the effect of saponins of Patrinia villosa against CRC cell has not been reported. In the current study, We have revealed that the effects of saponins of patrinia villosa on colorectal cancer (CRC) cell invasion and epithelial-mesenchymal transition (EMT) as well as its underlying mechanism.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Cadherin profiling for therapeutic interventions in Epithelial Mesenchymal Transition (EMT) and tumorigenesis

The major hallmarks of Epithelial-Mesenchymal Transition (EMT) is the loss of epithelial cell polarity and loss of expression of the cell- cell adhesion molecule like E-cadherin and acquired mesenchymal cells marker called N-Cadherin. This phenotypical changes of E-M plasticity of cells is extensively considered to be a crucial factor for tumor cells invasion and cancer metastasis; landmark events for transforming a locally growing tumor (benign tumor) into a systemic and live-threatening disease (malignant tumor). Cadherin molecules are adherens junction proteins and expressed as multiple isoforms. Cadherin switching occurs during normal tissue developmental processes; also recapitulates the increasing aggressive behavior and metastatic nature of cancer cells when E-Cadherin converts to N-Cadherin, in particular. There are several mechanisms established that cadherin switching and some of the underlying pathways involves multiple steps associated with migration and invasion of cancer cells, and finally colonization of micro metastatic lesions to form macro-metastasis. Inhibition of metastasis is complicated by the plasticity of cancer cells behaviors and the evolving nature of microenvironment. Although there is no clear evidence how that dynamic structural switching of cadherin family member occurs, stabilized and eventually influence cell behavior, phenotypic transformations and initiate tumorigenesis. Therefore, we emphasize here the major functions of over 20 existing human cadherins in tissue integrity and stability as well as mechanistic understanding on recent work of cadherin ectodomain-mediated adhesion, functional studies of the cell-cell adhesion through key signaling intermediates interacting with other binding partners. We hope understanding on how the dynamic all existing cadherins influence the cell behavior can be targeted to design possible therapeutic interventions to combat its activity and prevent tumor cell growth, invasion and metastasis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2023

Generic EMT Modeling for IBR

In support of IEEE P2800.2, PNNL is developing an informative annex about “Generic EMT Modeling for IBR”. A literature review has been conducted, covering an IEEE Task Force, Cigre Working Group, IEEE standards, NERC reports, and research articles. In addition, the vendors of widely used simulation tools have been contacted to verify the availability of real-code models of inverters. Illustrative computer simulations will be conducted, once real-code models become accessible. If the simulation results of a real-code model are obtained, a comparative study will be performed.

97 MATHEMATICS AND COMPUTING↗
DOE OSTI2026

A PSCAD Library Component Featuring a Reduced-Order IBR Model for EMT-Based Fault Studies

This paper presents a fully implemented inverter reduce-order-model (ROM) in an EMT simulation (PSCAD) library component for direct user utilization in protection studies. The developed inverter ROM has the following features: Equivalent to a full IBR inverter model with positive- and negative-sequence current formulation and representation A python script is developed to fully automate this process, including training data generation, ROM parameter training, updating parameters, and model verification and validation. With this PSCAD ROM library component, protection engineers can utilize a trustworthy, accurate ROM for protection studies in an easy-to-use and streamlined manner.

24 POWER TRANSMISSION AND DISTRIBUTION↗