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DOE OSTI2025

EMT-TS Hybrid Simulation for Large Power Grids Considering IBR-Driven Dynamics

The escalating integration of inverter-based resources (IBRs) poses new challenges to power systems by introducing fast dynamics with higher frequencies, which may need to be simulated by an electromagnetic transient (EMT) program. As an alternative to conducting EMT simulations for the entire system, which is typically time consuming, hybrid simulation between EMT and phasor-domain transient stability (TS) can greatly reduce the computational burden while preserving the detailed fast dynamics in the EMT zone. This paper establishes an EMT-TS hybrid simulation platform using open-source tools, specifically ParaEMT, GridPACK, and HELICS, which are the EMT simulator, TS simulator, and interface framework, respectively. Case studies on the 240-bus Western Electricity Coordinating Council (WECC) system demonstrate that the developed ParaEMT-HELICS-GridPACK hybrid simulator can accurately capture both slow electromechanical and fast IBR-driven dynamics with a 2.4x speedup.

electromagnetic transient↗

DOE OSTI2018

Advanced EMT and Phasor-Domain Hybrid Simulation With Simulation Mode Switching Capability for Transmission and Distribution Systems

Conventional electromagnetic transient (EMT) and phasor do-main hybrid simulation approaches presently exist for transmission system level studies and their simulation efficiency is generally constrained by the EMT simulation. With an increasing number of distributed energy resources and non-conventional loads being installed in the distribution systems, it is imperative to ex-tend the hybrid simulation application to include distribution systems and integrated transmission and distribution systems. Meanwhile, it is equally important to improve the simulation efficiency as the modeling scope and complexity of the detailed system in the EMT simulation increases. To meet both requirements, this paper introduces an advanced electromagnetic transient (EMT) and phasor domain hybrid simulation approach. This approach has two outstanding features: 1) a comprehensive phasor domain modeling framework which supports positive-sequence, three-sequence, three-phase and mixed three-sequence/three-phase representations; 2) a robust and flexible simulation mode switching scheme which enables simulation switching from hybrid simulation mode back to pure phasor domain dynamic simulation mode to achieve significantly improved simulation efficiency. The proposed method has been tested on integrated transmission and distribution systems, and the results show that with the developed simulation switching feature, the total computational time is significantly reduced compared to running the hybrid simulation for the whole simulation period, while good accuracy is maintained.

Huang, Qiuhua (ORCID:0000000184577429)↗

DOE OSTI2022

ParaEMT (NLR's (formerly known as NREL's) EMT Simulator: An Open Source, and HPC-Compatible Large-Scale Power System Electro-Magnetic Transient (EMT) Simulator) [SWR-22-16]

This open-source tool aims to provide a powerful and flexible platform for simulating electromagnetic transients (EMT) of large-scale inverter-based resource (IBR)-dominated power systems. The purpose of making it open source is to foster a community of EMT simulation and assist in exploring new EMT algorithms and applying advanced computational techniques to EMT simulation.

Tan, Jin↗

DOE OSTI2026

EMT Workshop Pre-session

The dataset contains installation instructions for the EMT Workshop 2026 with a python script and PSCAD file for verification of installation for the participants.

Sahu, Vibhuti [ORNL] (ORCID:000000034808527X)↗

NASA NTRS2010

High LET Radiation Can Enhance TGF(Beta) Induced EMT and Cross-Talk with ATM Pathways

The TGF(Beta) pathway has been shown to regulate or directly interact with the ATM pathway in the response to radiation in mammary epithelial cells. We investigated possible interactions between the TGF(Beta) and ATM pathways following simulated space radiation using hTERT immortalized human esophageal epithelial cells (EPC-hTERT), mink lung epithelial cells (Mv1lu), and several human fibroblast cell lines. TGF(Beta) is a key modulator of the Epithelial-Mesenchymal Transition (EMT), important in cancer progression and metastasis. The implication of EMT by radiation also has several lines of developing evidence, however is poorly understood. The identification of TGF(Beta) induced EMT can be shown in changes to morphology, related gene over expression or down regulation, which can be detected by RT-PCR, and immunostaining and western blotting. In this study, we have observed morphologic and molecular alternations consistent with EMT after Mv1lu cells were treated with TGF(Beta) High LET radiation enhanced TGF(Beta) mediated EMT with a dose as low as 0.1Gy. In order to consider the TGF(Beta) interaction with ATM we used a potent ATM inhibitor Ku55933 and investigated gene expression changes and Smad signaling kinetics. Ku559933 was observed to reverse TGF(Beta) induced EMT, while this was not observed in dual treated cells (radiation+TGF(Beta)). In EPC-hTERT cells, TGF(Beta) alone was not able to induce EMT after 3 days of application. A combined treatment with high LET, however, significantly caused the alteration of EMT markers. To study the function of p53 in the process of EMT, we knocked down P53 through RNA interference. Morphology changes associated with EMT were observed in epithelial cells with silenced p53. Our study indicates: high LET radiation can enhance TGF(Beta) induced EMT; while ATM is triggering the process of TGF(Beta)-induced EMT, p53 might be an essential repressor for EMT phenotypes.

Wang, Minli↗

DOE OSTI2018

NLRP3 inflammasome inhibition attenuates silica-induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells

Highlights: • Silica challenge dramatically induced EMT in line with NLRP3 inflammasome activation in 16HBE cells. • Genetic or pharmacological inhibition of NLRP3 inflammasome attenuated silica-induced EMT. • TAK1-MAPK-Snail/NF-κB pathway was involved in NLRP3 inflammasome mediated EMT process. • Pirfenidone exerted remarkable anti-EMT effect, which might be at least partially owing to its suppression of NLRP3 inflammasome. Silicosis is an incurable and progressive lung disease characterized by chronic inflammation and fibroblasts accumulation. Studies have indicated a vital role for epithelial-mesenchymal transition (EMT) in fibroblasts accumulation. NLRP3 inflammasome is a critical mediator of inflammation in response to a wide range of stimuli (including silica particles), and plays an important role in many respiratory diseases. However, whether NLRP3 inflammasome regulates silica-induced EMT remains unknown. Our results showed that silica induced EMT in human bronchial epithelial cells (16HBE cells) in a dose- and time-dependent manner. Meanwhile, silica persistently activated NLRP3 inflammasome as indicated by continuously elevated extracellular levels of interleukin-1β (IL-1β) and IL-18. NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT. Western blot analysis indicated that TAK1-MAPK-Snail/NF-κB pathway involved NLRP3 inflammasome-mediated EMT. Moreover, pirfenidone, a commercially and clinically available drug approved for treating idiopathic pulmonary fibrosis (IPF), effectively suppressed silica-induced EMT of 16HBE cells in line with NLRP3 inflammasome inhibition. Collectively, our results indicate that NLRP3 inflammasome is a promising target for blocking or retarding EMT-mediated fibrosis in pulmonary silicosis. On basis of this mechanism, pirfenidone might be a potential drug for the treatment of silicosis.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2022

Novel Real- Time EMT- TS Modeling Architecture for Feeder Blackstart Simulations

This paper presents the development and benchmarking of a novel real-time electromagnetic-transient and transient-stability (EMT-TS) modeling architecture for distribution feeder restoration studies. The work presents for the first time in the literature a real-time EMT-TS testbed in which the grid-forming unit is simulated in EMT domain, operating as the slack bus of the phasor domain while including unbalanced voltage conditions. To evaluate the performance and limitations of the proposed model, an equivalent EMT testbed is developed to serve as a benchmark. First, the co-simulation framework and the domain coupling methodology are introduced. Next, the steady state operation of the EMT-TS and EMT models are matched. Then, tests are conducted to analyze the transient performance of the proposed EMT-TS model when compared to its EMT benchmark. Results reveal that when utilizing a battery energy storage system (BESS) as the grid-forming unit, the EMT-TS testbed can maintain high accuracy for typical load steps.

Paduani, Victor↗

DOE OSTI2018

Induction of inactive TGF-β1 monomer formation by hydrogen sulfide contributes to its suppressive effects on Ang II- and TGF-β1-induced EMT in renal tubular epithelial cells

Highlights: • H{sub 2}S has anti-fibrotic actions with little information available about its mechanisms. • Ang II induced EMT in renal tubular epithelial cells via TGF-β. • H{sub 2}S inhibited Ang II- and TGF-β-induced EMT. • H{sub 2}S suppressed Ang II-induced activation of TGF-β. • H{sub 2}S inactivated TGF-β via cleavage of the disulfide bonds. Hydrogen sulfide (H{sub 2}S), an endogenous gas mediator with multifaced biological functions, has been shown to be effective in the prevention and treatment of renal sclerosis in several models of chronic renal diseases. The mechanisms involved are still unclear. Given that Ang II- and TGF-β-induced renal tubular epithelial-mesenchymal transition (EMT) is a pivotal cellular event leading to renal sclerosis, we examined whether and how H{sub 2}S intervened the processes of EMT. Ang II stimulated EMT in renal tubular epithelial cells, as indicated by the increased level of α-smooth muscle actin and a decreased level of E-cadherin. This effect of Ang II was blocked by a TGF-β receptor kinase inhibitor, indicative of a mediating role of TGF-β. Consistently, Ang II stimulated TGF-β activation and addition of the exogenous TGF-β1 also induced EMT. In the presence of H{sub 2}S donor NaHS, the EMT-promoting actions of Ang II and TGF-β1 were abolished, which was associated with a reduced TGF-β activity. Further analysis using a human recombinant active TGF-β1 revealed that H{sub 2}S cleaved the disulfide bond in the dimeric active TGF-β1 and promoted the formation of inactive TGF-β1 monomer. Collectively, these results indicate that H{sub 2}S counteracted Ang II- and TGF-β1-induced EMT through mechanisms involving direct inactivation of TGF-β1. Our study thus provides novel mechanistic insight into the anti-fibrotic actions of H{sub 2}S and suggest that H{sub 2}S could be used to treat renal sclerotic diseases.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Simvastatin inhibits the development of radioresistant esophageal cancer cells by increasing the radiosensitivity and reversing EMT process via the PTEN-PI3K/AKT pathway

Highlights: • Radioresistant Ec9706-R cells acquire EMT characteristics. • Simvastatin restores the sensitivity of Ec9706-R to irradiation. • Simvastatin suppresses irradiation-induced EMT. • PTEN-PI3K/AKT pathway involves in simvastatin-induced radiosensitivity, EMT reversion. • Simvastatin aggravates radiation-inhibited radioresistant EC xenograft tumor growth. Acquired radioresistance compromises the efficacy of radiotherapy for carcinomas including esophageal cancer (EC), thus resulting in recurrence and poor survival. Recent research corroborated radiosensitive function of simvastatin in stem-like breast cancer cells. However, its role in EC radioresistance remains poorly elucidated. Here, we developed a radioresistant EC cell line Ec9706-R with higher resistance to irradiation relative to control Ec9706 cells. Intriguingly, Ec9706-R cells exhibited epithelial-mesenchymal transition (EMT) characteristics with high invasion and migration ability. Simvastatin sensitized radioresistance of Ec9706-R cells and suppressed cell proliferation, but aggravated radiation-induced apoptosis and caspase-3 activity. Furthermore, simvastatin reversed EMT and inhibited cell invasion and migration of Ec9706-R cells. Mechanism assay confirmed the activation of PI3K/AKT pathway after radiation, which was inhibited by simvastatin. After restoring this pathway by its activator, IGF-1, simvastatin-mediated radiosensitivity and EMT reversion were abrogated. Further assay substantiated the PTEN suppression after irradiation, which was elevated following simvastatin pre-treatment. Moreover, PTEN cessation attenuated the inhibitory effect of simvastatin on PI3K/AKT activation, and subsequently antagonized simvastatin-induced radiosensitivity and EMT reversion. Additionally, simvastatin aggravated radiation-mediated Ec9706-R tumor growth inhibition. Together, simvastatin inhibits the development of Ec9706-R cells by increasing radiosensitivity and reversing EMT via PTEN-PI3K/AKT pathway, implying a promising strategy against EC radioresistance.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2025

RE-INTEGRATE EMT Simulation Software: DAE Solvers and Automation

Existing electromagnetic transient (EMT) simulation tools face challenges in accelerating EMT simulations, especially for very large-scale power networks. To tackle this issue, next generation EMT simulation tools such as RE-INTEGRATE EMT are being researched upon. Such tools should be equipped with automation capabilities and advanced numerical differential-algebraic equation (DAE) solvers. In this paper, the DAE solvers incorporated within the RE-INTEGRATE EMT simulation tool are discussed. In particular, a modified ODEINT-based DAE solver and the ARKODE solver from SUN-DIALS are leveraged within RE-INTEGRATE EMT. In addition, the automation implemented within RE-INTEGRATE EMT to automate the DAE generation (replacing the need of manual discretization and assembling DAEs) is discussed. Different use cases were implemented using the RE-INTEGRATE EMT tool and were validated with respect to baseline simulations.

Marthi, Phani Ratna Vanamali [ORNL] (ORCID:0000000↗

DOE OSTI2024

EMT data generation

The integration of inverter-based resources (IBRs) in power systems is accelerating, bringing with it significant benefits such as reduced greenhouse gas emissions, improved grid resilience, and increased energy independence. Despite these advantages, the widespread adoption of IBRs introduces several challenges, including issues related to grid stability, increased operational complexity, and the need for updated regulatory frameworks. To address these challenges, IEEE released Standard 2800 in 2022, which sets forth the necessary interconnection capabilities and performance criteria for IBRs connected to transmission and sub-transmission systems. This standard outlines the performance requirements to ensure the reliable integration of IBRs into the bulk power system. Furthermore, in 2023, the North American Electric Reliability Corporation (NERC) published a reliability guideline for electromagnetic transient (EMT) modeling of BPS-connected IBRs. This guideline provides recommendations for developing EMT model requirements, performing model quality checks, and implementing verification practices specifically for EMT models representing BPS-connected inverter-based resources in reliability studies conducted by transmission planners and planning coordinators. These standards and guidelines have a profound impact on EMT studies for transmission networks, influencing system stability analyses, grid recovery and resynchronization processes, fault ride-through evaluations, protection and coordination strategies, advanced control methodologies, and the inclusion of IBRs in transient models of transmission networks. As a result, the generation of EMT data is crucial for conducting various transient-based studies to understand the impact of IBRs. EMT data generation use cases serve as the basis for scenarios in event detection and identification use cases, providing comprehensive details about EMT data generation for transmission grids with inverter-based resources. These use cases supply sufficient training and validation datasets for subsequent EMT analysis algorithms.

Xia, Qianxue↗

DOE OSTI2022

Common Information Model for Electromagnetic Transients (CIM for EMT): CRADA 533 [Abstract only}

The control and protection functions of inverter-based resources (IBR) have raised concerns with bulk system reliability. Most of the current interest lies with solar photovoltaic generation but increasing amounts of storage would pose the same risks. Newer North American Electric Reliability Corporation (NERC) guidelines call for electromagnetic transient (EMT) studies of IBR and recommend that transmission operators collect distributed energy resource (DER) data to support such modeling. IEEE Standard P2800.1 is defining tests for model parameterization, so good model data should become available from inverter vendors. (EMT studies also apply to large power transformer reliability, and transformer vendors can provide EMT models.) Utilities don’t currently have the rest of the bulk system represented for EMT studies at large scale. An International Electrotechnical Commission (IEC) standard Common Information Model (CIM) provides a way of supporting these detailed models from physical asset data, e.g., conductors, towers, transformer data sheets, control block diagrams, while avoiding software vendor lock-in. CIM-for-EMT, with proposed schema extensions and open-source converters, provides a way to exchange EMT data between organizations and tools. This project leverages Office of Electricity (OE) funding of CIM-for-EMT code base through the GridAPPS-DTM project, and of GridPACKTM (parallelized transmission solver), for interoperability testing in CIM-for-EMT. The project also leverages partner PGSTech investments in EMTP® interoperability with CIM.

24 POWER TRANSMISSION AND DISTRIBUTION↗

DOE OSTI2019

Advanced High-Fidelity Lumped EMT Grid Modelling & Comparison

There is increased interest in performing electromagnetic transient (EMT) studies of large power grids for stability purposes. The large power grids may not represent the entire grid, but portions of interest. For example, studies are being performed to identify the impact of extreme events on solar power plants in California that requires the EMT model of the grid in California, but not the complete western interconnection (WI) grid model to which the grid in California is connected. The EMT models of grids are necessary to perform integration studies of large power electronics systems like utility-scale photovoltaic (PV) systems, high-voltage direct current (HVdc) systems, flexible alternating current transmission systems (FACTs), and others. Traditionally, models of grids available to utilities are the transient stability (TS) models. Hence, it assumes significance to identify methods of developing high-fidelity EMT models for portions of the grid (of interest) from the information available in the existing TS models of the entire grid. In this paper, a conversion mechanism along with upgradation based on data-driven methods is applied to develop EMT models of grids. The conversion mechanism utilizes information from TS models of grids to generate EMT models of grids. These models can be extracted for the required portion of the grid. While these models adequately represent the local voltage behaviour of the grid, they are inadequate in representing the frequency behaviour of the grid. The data-driven methods are applied to identify frequency dynamics of the grid, and the EMT models are upgraded with the data-driven methods. The resulting upgraded EMT models of grids can perform the studies mentioned above. These models are tested under contingencies of interest to validate the developed models.

Debnath, Suman↗

DOE OSTI2018

EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database

Highlights: • Integrated analysis identifies EMT-associated lncRNA in HCC. • Candidate lncRNA-associated genes are enriched in EMT-linked pathways. • LncRNA WDFY3-AS3, MIAT, and MEG3 contribute to the EMT phenotype of HCC cells. Accumulating evidence suggest that dysregulated expression of long non-coding RNA (lncRNA) plays a critical role in human tumorigenesis. However, little is known about the lncRNA implicated in the epithelial-to-mesenchymal transition (EMT) process. In this study, we performed data mining in The Cancer Genome Atlas (TCGA) hepatocellular carcinoma (HCC) data set and identified the a spectrum of differentially expressed lncRNAs implicated the EMT process of HCC, and functionally validated their roles in LM3 cells. Especially, lncRNA WDFY3-AS2-, LINC00472-, MIAT-, and MEG3-associated genes were significantly enriched in EMT-linked pathways. Loss-of-function study showed that genetic silencing of WDFY3-AS3, MIAT, and MEG3, but not LINC00472, resulted in reduced N-cadherin expression, cell migration, and cell invasion. Collectively, our results identify several lncRNAs that regulate the EMT process of HCC, which provides critical information for HCC tumorigenesis and potential therapeutic targets.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

High mobility group A2 (HMGA2) promotes EMT via MAPK pathway in prostate cancer

Highlights: • HMGA2 expression increases with prostate cancer progression. • Wild-type HMGA2 promotes EMT via MAPK. • Truncated HMGA2 increases cell viability and migration via non-EMT pathway. Studies have shown that High mobility group A2 (HMGA2), a non-histone protein, can promote epithelial-mesenchymal transition (EMT), which plays a critical role in prostate cancer progression and metastasis. Interestingly, full-length or wild-type HMGA2 and truncated (lacking the 3′UTR) HMGA2 isoforms are overexpressed in several cancers. However, there are no studies investigating the expression and differential roles of WT vs truncated HMGA2 isoforms in prostate cancer. Immunohistochemical staining of prostate tissue microarray revealed low membrane expression in normal epithelial prostate cells, and that expression increased with tumor grade as well as a switch from predominantly cytoplasmic HMGA2 in lower tumor grades, to mostly nuclear in high grade and bone metastatic tissue. LNCaP cells stably overexpressing wild-type HMGA2 displayed nuclear localization of HMGA2 and induction of EMT associated with increased Snail, Twist and vimentin expression compared to LNCaP Neo control cells, as shown by immunofluorescence and western blot analyses. This was associated with increased cell migration on collagen shown using boyden chamber assay. Conversely, LNCaP cells overexpressing truncated HMGA2 showed cytoplasmic HMGA2 expression that did not induce EMT yet displayed increased cell proliferation and migration compared to LNCaP Neo. Both wild-type and truncated HMGA2 increased levels of phospho-ERK, and interestingly, treatment with U0126, MAPK inhibitor, antagonized wild-type HMGA2-mediated EMT and cell migration, but did not affect truncated HMGA2-mediated cell proliferation or migration. Therefore, although both wild-type and truncated HMGA2 may promote prostate tumor progression, wild-type HMGA2 acts by inducing EMT via MAPK pathway.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2017

Impaired autophagic flux and p62-mediated EMT are involved in arsenite-induced transformation of L-02 cells

Autophagy is a catabolic process essential for preserving cellular homeostasis, and the epithelial-to-mesenchymal transition (EMT) is involved during tissue development and cancer progression. In arsenite-treated human hepatic epithelial (L-02) cells, arsenite reduced the autophagic flux, which caused accumulation of p62, an adaptor and receptor of autophagy. Further, in arsenite-transformed L-02 cells, the levels of E-cadherin were attenuated, but the levels of vimentin, which is expressed in mesenchymal cells, and Snail, a transcription regulator of the EMT, were up-regulated. Thus, after chronic exposure of L-02 cells to arsenite, the impaired autophagic flux induced the accumulation of p62, which up-regulated the expression of Snail, a protein involved in arsenite-induced EMT of these cells. Knockdown of p62 by siRNA reversed the arsenite-induced EMT and decreased the capacities of arsenite-transformed L-02 cells for colony formation and invasion and migration. Therefore, in arsenite-induced transformation of L-02 cells, the accumulation of p62, by impairing autophagic flux, mediates the EMT via Snail. These results provide a previously unknown mechanism underlying arsenic toxicity and carcinogenicity. - Highlights: • Impaired autophagic flux induces the accumulation of p62 in arsenite-treated L-02 cells. • The EMT is associated with arsenite-induced transformation in L-02 cells. • p62 mediates the EMT via Snail in arsenite-induced transformation of L-02 cells.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Oxaliplatin and irinotecan induce heterogenous changes in the EMT markers of metastasizing colorectal carcinoma cells

Highlights: • Significant variability and lower expression uniformity in lymph node metastatic cells. • Heterogeneity of cell response partially determined by cancer cell microenvironment. • Metastatic cells proved to be less sensitive to chemotherapy treatment compared to primary site cancer cells. • Irinotecan and oxaliplatin affected EMT markers in primary cell lines. In patients with advanced colorectal cancer (CRC), surgery is complemented with systemic therapy – chemotherapy and radiochemotherapy. Although the patients’ overall survival has been significantly improved, tumor resistance is still a frequent cause of chemotherapy failure. Several factors contribute to chemoresistance of tumor cells including changes related with epithelial-mesenchymal transition (EMT). The present study was designed to verify the presence of EMT markers in paired CRC primary cell lines obtained from primary tumor sites and lymph node metastases of three patients and to investigate the effect of irinotecan and oxaliplatin treatment on these markers as well. The samples of the higher stage of CRC and positive for angioinvasion were selected and qPCR, western blot analysis, migration assay, cytotoxicity testing was performed. Results confirmed the increased expression of several markers characteristic of EMT and invasiveness in lymph node metastatic cells, with a significant variability between individual samples. Irinotecan and oxaliplatin decreased migration activity of the cells and to the varying degree affected the expression of EMT and invasiveness markers. In conclusion, in CRC EMT is present in metastatic cells over a phenotypic continuum whose expression is altered heterogeneously upon irinotecan and oxaliplatin treatment.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

FPPS mediates TGF-β1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway

Highlights: • FPPS expression is significantly correlated with TNM stage and metastasis of non-small cell lung cancer. • Inhibition or knockdown of FPPS blocks TGF-β1-induced cell invasion and EMT. • FPPS expression is induced by TGF-β1. • FPPS mediates TGF-β1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-β1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-β1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-β1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.

60 APPLIED LIFE SCIENCES↗