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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 1,603 records · Page 89
All sourcesNASA NTRSDOE OSTI
DOE OSTI2016

Implementation of the direct S ( α , β ) method in the KENO Monte Carlo code

The Monte Carlo code KENO contains thermal scattering data for a wide variety of thermal moderators. These data are processed from Evaluated Nuclear Data Files (ENDF) by AMPX and stored as double differential probability distribution functions. The method examined in this study uses S(α,β) probability distribution functions derived from the ENDF data files directly instead of being converted to double differential cross sections. This allows the size of the cross section data on the disk to be reduced substantially amount. KENO has also been updated to allow interpolation in temperature on these data so that problems can be run at any temperature. Results are shown for several simplified problems for a variety of moderators. In addition, benchmark models based on the KRITZ reactor in Sweden were run, and the results are compared with the previous versions of KENO without the direct S(α,β) method. Results from the direct S(α,β) method compare favorably with the original results obtained using the double differential cross sections. Finally, sampling the data increases the run-time of the Monte Carlo calculation, but memory usage is decreased substantially.

73 NUCLEAR PHYSICS AND RADIATION PHYSICS↗
DOE OSTI2018

Dynamic event tree analysis with the SAS4A/SASSYS-1 safety analysis code

The consequences of a transient in an advanced sodium-cooled fast reactor are difficult to capture with the traditional approach to probabilistic risk assessment (PRA). Numerous safety-relevant systems are passive and may have operational states that cannot be represented by binary success or failure. In addition, the specific order and timing of events may be crucial which necessitates the use of dynamic PRA tools such as ADAPT. The modifications to the SAS4A/SASSYS-1 sodium-cooled fast reactor safety analysis code for linking it to ADAPT to perform a dynamic PRA are described. A test case is used to demonstrate the linking process and to illustrate the type of insights that may be gained with this process. Finally, newly-developed dynamic importance measures are used to assess the significance of reactor parameters/constituents on calculated consequences of initiating events.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗
DOE OSTI2019

Continuous-energy Monte Carlo neutron transport on GPUs in the Shift code

Here, a continuous-energy Monte Carlo neutron transport solver executing on GPUs has been developed within the Shift code. Several algorithmic approaches are considered, including both history-based and event-based implementations. Unlike in previous work involving multigroup Monte Carlo transport, it is demonstrated that event-based algorithms significantly outperform a history-based approach for continuous-energy transport as a result of increased device occupancy and reduced thread divergence. Numerical results are presented for detailed full-core models of a small modular reactor (SMR), including a model containing depleted fuel materials. These results demonstrate the substantial gains in performance that are possible with the latest-generation of GPUs. On the depleted SMR core configuration, an NVIDIA P100 GPU with 56 streaming multiprocessors provides performance equivalent to 90 CPU cores, and the latest V100 GPU with 80 multiprocessors offers the performance of more than 150 CPU cores.

73 NUCLEAR PHYSICS AND RADIATION PHYSICS↗
DOE OSTI2019

Modeling a fast spectrum molten salt reactor in a systems dynamics fuel cycles code

Molten salt reactor (MSR) concepts are being actively developed by several private companies, with some touting the fuel cycle benefits of this technology. Simulating the deployment of MSRs and their effect on fuel cycle transitions is the role of a system dynamics fuel cycles tool. However, many current fuel cycles tools have difficulty modeling MSR isotopic variations because they were designed for modeling existing reactors based on discrete fuel elements with batch fueling schemes (i.e., charge and discharge). This work presents ORION fuel cycle modeling results using a specific high power density fast spectrum MSR design. For code verification, a single-stage MSR fuel cycle was set up in ORION and results were compared with the results from the SCALE-based reactor physics model (ChemTriton). A transition scenario was set up in ORION from the current light water reactor fleet to a future fleet of MSRs to study the characteristics of an MSR that affect its performance during transition. Several transition scenarios were set with holds and delays in place that are representative of a sodium fast reactor as modeled in Evaluation Group 23 for the Fuel Cycle Options Campaign Evaluation and Screening Study. Several MSR characteristics lend to its high performance and ease in transition from the current fuel cycle: fissile material is only loaded at initial startup; all fissile material is available as it is bred due to online fuel processing; and fissile material recirculating through the core is briefly held in tanks for processing and has very minimal out-of-core time (on the order of a minutes to a few days). These characteristics are in contrast to a solid-fueled reactor, which requires discharge, cooling, and fabrication of fuel all of which could take a few months to a few years and repeated loading of fresh fuel assemblies. In conclusion, a solid-fueled reactor only discharges a fraction of a core every year.

11 NUCLEAR FUEL CYCLE AND FUEL MATERIALS↗
DOE OSTI2020

ONIX: An open-source depletion code

Open Source software enables innovative, community-based software development. ONIX brings this concept to the field of depletion calculations. It is an open-source depletion software to be used for nuclear reactor simulations, for fissile material production analysis as well as for nuclear arms control applications. ONIX provides a module to solve the depletion equation using a Chebyshev Rational Approximation Method. For the generation of one-group cross sections, it includes a coupling interface for the open-source neutron transport code, OpenMC, as well as a module to read pre-computed values in a stand-alone mode. ONIX has special features to optimize nuclear data libraries, to update isomeric branching ratio during burnup, and to support automation of simulations for nuclear archaeology. In conclusion, ONIX has been validated against results from numerical and experimental benchmarks, and its results agree with other methods within expected error ranges.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗
DOE OSTI2021

Domain decomposition in the GPU-accelerated Shift Monte Carlo code

The GPU solver within the Shift continuous-energy Monte Carlo neutron transport code has been extended to provide domain decomposition in addition to domain replication to enable the solution of problems with memory requirements exceeding the capacity of a single GPU. The strategy follows the Multiple Set, Overlapping Domain (MSOD) approach that is used in Shift’s CPU solver and integrates into the event-based algorithm used for Shift’s GPU solver. Furthermore, the ability to assign processors to spatial domains non-uniformly has been maintained. In this work, two different approaches for communicating particle data between domains are considered, and multiple criteria for load balancing problems have been investigated. Numerical results are presented for both fresh and depleted small modular nuclear reactor (SMR) cores. A parallel efficiency of approximately 80% was achieved with up to 16 spatial domains measured relative to full domain replication. A scaling study on the Summit supercomputer demonstrates a weak scaling parallel efficiency of over 90% on over 24000 GPUs.

97 MATHEMATICS AND COMPUTING↗
DOE OSTI2023

Benchmarking FFTF LOFWOS Test# 13 using SAM code: Baseline model development and uncertainty quantification

The development and deployment of advanced reactors, such as the sodium-cooled fast reactor (SFR), relies on sophisticated modeling tools to ensure the safety of the design under various transients. The predictive capability of these advanced modeling tools requires validation to garner trust in supporting the licensing of the advanced reactors. For this reason, the International Atomic Energy Agency (IAEA) initiated a coordinated research project (CRP) in 2018 for the analysis of the Fast Flux Test Facility (FFTF) Loss of Flow Without Scram (LOFWOS) Test #13.In this study, we present and discuss the benchmarking efforts of the modern system code SAM on the FFTF LOFWOS Test #13. Further, the SAM baseline model was developed according to the benchmark specification, which included a detailed core model with reactivity feedback. Generally, good agreement was observed between the baseline results and benchmark measurements; however, discrepancies persisted, particularly in predicted fuel assembly coolant outlet temperatures. Utilizing the baseline model, uncertainty quantification (UQ) and sensitivity analysis (SA) were conducted with the assistance of various statistical learning and machine learning methods, including kernel density estimation, Gaussian processes, and Sobol indices. Following the baseline model prediction and UQ and SA results, we discuss the reasons for the simulation discrepancies and propose further improvements to the model. This benchmarking effort adheres to the best-estimate plus uncertainty approach and can serve as a valuable example for supporting risk-informed licensing of advanced reactors.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗
DOE OSTI2016

The two-qubit amplitude damping channel: Characterization using quantum stabilizer codes

A protocol based on quantum error correction based characterization of quantum dynamics (QECCD) is developed for quantum process tomography on a two-qubit system interacting dissipatively with a vacuum bath. The method uses a 5-qubit quantum error correcting code that corrects arbitrary errors on the first two qubits, and also saturates the quantum Hamming bound. The dissipative interaction with a vacuum bath allows for both correlated and independent noise on the two-qubit system. We study the dependence of the degree of the correlation of the noise on evolution time and inter-qubit separation.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗
DOE OSTI2014

Long non-coding RNA Loc554202 regulates proliferation and migration in breast cancer cells

Highlights: • First, we have shown that upregulated of the Loc554202 in breast cancer tissues. • Second, we demonstrated the function of Loc554202 in breast cancer cell. • Finally, we demonstrated that LOC554202 knockdown could inhibit tumor growth in vivo. - Abstract: Data derived from massive cloning and traditional sequencing methods have revealed that long non-coding RNAs (lncRNA) play important roles in the development and progression of cancer. Although many studies suggest that the lncRNAs have different cellular functions, many of them are not yet to be identified and characterized for the mechanism of their functions. To address this question, we assay the expression level of lncRNAs–Loc554202 in breast cancer tissues and find that Loc554202 is significantly increased compared with normal control, and associated with advanced pathologic stage and tumor size. Moreover, knockdown of Loc554202 decreased breast cancer cell proliferation, induced apoptosis and inhibits migration/invasion in vitro and impeded tumorigenesis in vivo. These data suggest an important role of Loc554202 in breast tumorigenesis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Long non-coding RNA HOTAIR promotes carcinogenesis and invasion of gastric adenocarcinoma

Highlights: • HOTAIR expression was tested in fifty patients with gastric cancer. • Cell proliferation was measured after HOTAIR silencing in gastric cancer cell line. • siRNA–HOTAIR suppresses cell invasiveness and capacity of migration. • Knock down of HOTAR leads to decreased expression of EMT markers. • Inhibition of HOTAIR induces apoptosis and cell cycle arrest. - Abstract: Gastric cancer is one of the major causes of cancer death worldwide; however, the mechanism of carcinogenesis is complex and poorly understood. Long non-coding RNA HOTAIR (HOX transcript antisense RNA) recently emerged as a promoter of metastasis in various cancers including gastric cancer. Here we investigated the impact of HOTAIR on apoptosis, cell proliferation and cell cycle to dissect the carcinogenesis of gastric cancer. We examined the mechanism of invasion and metastasis and analyzed the clinical significance of HOTAIR. Downregulation of HOTAIR was confirmed by two different siRNAs. The expression of HOTAIR was significantly elevated in various gastric cancer cell lines and tissues compared to normal control. si-HOTAIR significantly reduced viability in MKN 28, MKN 74, and KATO III cells but not in AGS cells. si-HOTAIR induced apoptosis in KATO III cells. Lymphovascular invasion and lymph node metastasis were more common in the high level of HOTAIR group. si-HOTAIR significantly decreased invasiveness and migration. si-HOTAIR led to differential expression of epithelial to mesenchymal transition markers. We found that HOTAIR was involved in inhibition of apoptosis and promoted invasiveness, supporting a role for HOTAIR in carcinogenesis and progression of gastric cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-κB1

Background and objective: Long non-coding RNA, BANCR, has been demonstrated to contribute to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer is still unknown. In present study, we investigated whether BANCR was involved in the development of gastric cancer cells via regulation of NF-κB1. Methods: Human gastric cancer tissues were isolated as well as human gastric cell lines MGC803 and BGC823 were cultured to investigate the role of BANCR in gastric cancer. Results: BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-κB1 (P50/105) expression and 3′UTR of NF-κB1 activity. Overexpression of NF-κB1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-κB1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis. Conclusion: BANCR was highly expressed both in gastric tumor tissues and in cancer cells. NF-κB1 and miR-9 were involved in the role of BANCR in gastric cancer cell growth and apoptosis. - Highlights: • BANCR up-regulated in gastric cancer (GC) tissues and cell lines MGC803 and BGC823. • Down-regulation of BANCR inhibited GC cell growth and promoted cell apoptosis. • Down-regulation of BANCR contributed to decreased 3′UTR of NF-κB1 and its expression. • Overexpressed NF-κB1 reversed the effect of BANCR on GC cell growth. • miR-9 inhibitor reversed the effect of BANCR on cancer GC cell growth.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Long non-coding RNA lnc-MX1-1 is associated with poor clinical features and promotes cellular proliferation and invasiveness in prostate cancer

Long non-coding RNAs (lncRNAs) are emerging as key molecules in human cancer genesis and progression, including prostate cancer. Large amount of lncRNAs have been found that differentially expressed between prostate cancer tissues and normal prostate tissues. Whether these lncRNAs could serve as a novel biomarker for prostate cancer diagnosis or prognosis, and their biological functions in prostate cancer need further investigation. In the present study, we identified that lncRNA lnc-MX1-1 is over-expressed in prostate cancer tissues compared with their adjacent normal prostate tissues by gene expression array profiling. The expression of lnc-MX1-1 in 60 prostate cancer cases was determined by real-time quantitative PCR and the correlations between lnc-MX1-1 expression and patients' clinical features were further analyzed. Next, we impaired lnc-MX1-1 expression using RNAi in LNCaP and 22Rv1 prostate cancer cells to explore the effects of lnc-MX1-1 on proliferation and invasiveness of the cells. Our results showed that there was a significant association between over-expression of lnc-MX1-1 and patients' clinical features such as PSA, Gleason score, metastasis, and recurrence free survival. Moreover, knockdown of lnc-MX1-1 reduced both proliferation and invasiveness of LNCaP and 22Rv1 cells. In conclusion, the results suggest that lnc-MX1-1 may serve as a potential biomarker and therapeutic target for prostate cancer. - Highlights: • LncRNA lnc-MX1-1 is up-regulated in prostate cancer. • Overexpression of lnc-MX1-1 is correlated with poor prostate cancer clinical features. • Knockdown of lnc-MX1-1 reduces proliferation and invasiveness of prostate cancer cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation, migration and invasion by depending on p53’s transcriptional activity

Long non-coding RNAs (lncRNAs) was found to play critical roles in tumorigenesis, hence, screen of tumor-related lncRNAs, identification of their biological roles is important for understanding the processes of tumorigenesis. In this study, we identified the expressing difference of several tumor-related lncRNAs in breast cancer samples and found that, MEG3, which is downregulated in non-small cell lung cancer (NSCLC) tumor tissues, is also downregulated in breast cancer samples compared with adjacent tissues. For figuring out the effect of MEG3 in breast cancer cells MCF7 and MB231, we overexpressed MEG3 in these cells, and found that it resulted the inhibition of proliferation, colony formation, migration and invasion capacities by enhancing p53’s transcriptional activity on its target genes, including p21, Maspin and KAI1. MEG3 presented similar effects in MB157, which is a p53-null breast cancer cell line, when functional p53 but not p53R273H mutant, which lacks transcriptional activity, was introduced. Surprisingly, overexpression of MEG3 activates p53’s transcriptional activity by decreasing MDM2’s transcription level, and thus stabilizes and accumulates P53. Taken together, our findings indicate that MEG3 is downregulated in breast cancer tissues and affects breast cancer cells’ malignant behaviors, which indicate MEG3 a potential therapeutic target for breast cancer. - Highlights: • MEG3 RNA is widely downregulated in breast tumor tissue. • MEG3 regulates P53 indirectly through transcriptional regulation of MDM2. • Under unstressed condition, MEG3-related P53 accumulation transcriptionally activates p53’s target genes. • MEG3 expression level tightly regulates proliferation, colony formation, migration and invasion in breast tumor cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Long non-coding RNA linc-cdh4-2 inhibits the migration and invasion of HCC cells by targeting R-cadherin pathway

Long non-coding RNAs (LncRNAs) have played very important roles in the malignancy behaviors of hepatocellular carcinoma (HCC). Linc-cdh4-2 (TCONS-00027978) is a novel LncRNA that has been identified in HCC tissues from our previous study. Overexpression of linc-cdh4-2 in HCC cell lines (SK-Hep-1 and Huh7) significantly decreases the migration and invasion abilities of these cells, while knockdown the expression of linc-cdh4-2 significantly increases the migration and invasion abilities. Interestingly, neither the over expression nor the knock down of linc-cdh4-2 could affect the viability and proliferation of HCC cells. Mechanistically, the linc-cdh4-2 could up-regulate the protein level of R-cadherin through direct binding that might improve the protein stability. Over expression of linc-cdh4-2 could significantly increase the protein levels of R-cadherin and decrease the protein levels of small GTPase RAC1, and vice-versa. Further knockdown R-cadherin in linc-cdh4-2 stably overexpressed cells, could significantly upregulate the protein levels of RAC1 and improve the cell migration and invasion abilities. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway. - Highlights: • Linc-cdh4-2 negatively related with the invasion and metastasis ability of HCC cells. • Linc-cdh4-2 could up-regulate the protein level of R-cadherin through direct binding. • Knockdown of R-cadherin increases the migration and invasion abilities of HCC cell. • Knockdown of R-cadherin could significantly upregulate the protein levels of RAC1.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p

Recently, long non-coding RNAs (lncRNAs) have been shown to have critical regulatory roles in tumourigenesis. Increasing evidence has suggested that lncRNA NEAT1 has been implicated in various types of human cancer. However, the potential biological roles and regulatory mechanisms of NEAT1 in pancreatic cancer (PC) remains unclear. Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. Besides, our findings indicate that high NEAT1 expression level is closely correlated with tumor progression and poor survival in PC patients. Furthermore, we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers. Additionally, our results confirmed that the tumor-promoting effects of NEAT1 in PC cells is at least partly through negative modulation of miR-506-3p. Overall, our results suggested that NEAT1 functions as an oncogenic lncRNA in PC, which could be a novel diagnostic and therapeutic target for PC. - Highlights: • Upregulation of NEAT1 expression was significantly associated with the poor survival in PC patients. • Knockdown of NEAT1 can suppress PC cells growth by inducing cell cycle arrest and apoptosis promotion in vitro study. • NEAT1 functions as an oncogene in pancreatic cancer by acting as a competing endogenous RNA for miR-506-3p. • The tumor-suppressive effects of NEAT1 knockdown in PC cells was partially reversed by miR-506-3p inhibitor.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Bimodal expression of yeast GAL genes is controlled by a long non-coding RNA and a bifunctional galactokinase

Bimodality in gene expression can generate phenotypic heterogeneity facilitating fitness and growth of isogenic cell populations in suboptimal environments. We investigated the mechanism by which, in conditions of limiting galactose, yeast cell populations activate GAL genes in a bimodal fashion with a cell fraction expressing GAL genes (ON), while the rest subpopulation is kept at the non-expressing (OFF) state. We show that a long non-coding RNA (GAL10-ncRNA) crossing the bidirectional GAL1-10 promoter, decreases the rate by which single cells commit transition to the ON state without affecting the rate of GAL transcription per se in ON cells. This is accomplished by repressing stochastic expression of the bifunctional Gal1p galactokinase, which besides its enzymatic activity acts as an essential inducer of the system under those conditions. We show that once single cells switch to the ON state, the GAL10-ncRNA effect is overridden by accumulating Gal1p levels sufficient to feedback positively on Gal4p, and not by the active transcription of GAL10 that occurs in opposite direction relative to that of GAL10-ncRNA. Conversely, GAL10-ncRNA does not influence transition of ON cells, where Gal4p is active, back to the OFF state. Our model suggests that the functional interplay between GAL10-ncRNA transcription, stochastic Gal1p expression and Gal1p positive feedback on Gal4p constitutes a novel molecular switch mechanism dictating the commitment of individual cells for either metabolic state. - Highlights: • Stochastic transcription of the Gal1p galactokinase creates bimodality in GAL expression. • GAL10-ncRNA controls GAL bimodality by repressing Gal1p. • GAL10-ncRNA repression is overridden by the inducing activity of Gal1p itself.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203

Long non-coding RNAs (lncRNAs) have emerged as critical regulators of the progression of human cancers, including colorectal cancer (CRC). The study of genome-wide lncRNA expression patterns in metastatic CRC could provide novel mechanism underlying CRC carcinogenesis. In here, we determined the lncRNA expression profiles correlating to CRC with or without lymph node metastasis (LNM) based on microarray analysis. We found that 2439 lncRNAs and 1654 mRNAs were differentially expressed in metastatic CRC relative to primary CRC. Among these dysregulated lncRNAs, FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors. Functionally, knockdown of FBXL19-AS1 played tumor-suppressive effects by inhibiting cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo. Overexpression of FBXL19-AS1 was markedly correlated with TNM stage and LNM in CRC. Bioinformatics analysis predicted that miR-203 was potentially targeted by FBXL19-AS1, which was confirmed by dual-luciferase reporter assay. Pearson's correlation analysis showed that miR-203 expression was negatively related to FBXL19-AS1 in tumor tissues. Finally, miR-203 inhibition abrogated the effect of FBXL19-AS1 knockdown on the proliferation and invasion of LoVo cells. Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development. - Highlights: • LncRNA expression signature was different between metastatic and primary tumors. • Knockdown of FBXL19-AS1 inhibits proliferation, migration and invasion in vitro. • Knockdown of FBXL19-AS1 inhibits tumorigenesis and metastasis in vivo. • FBXL19-AS1 was upregulated in CRC tissues and related with lymph node metastasis. • FBXL19-AS1, acting as a molecular sponge in negatively regulating miR-203.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma

Recently, long noncoding RNAs (lncRNAs) have been reported to have crucial regulatory efficiency in human cancer biology. Long intergenic non-coding RNA 668 (LINC00668) was regarded as an oncogene in multiple cancers. However, the underlying molecular mechanism of LINC00668 in oral squamous cell carcinoma (OSCC) has not been studied. In this study, we first demonstrated that LINC00668 expression was up-regulated, which was correlated with tumor progression, and miR-297 down-regulated in OSCC tissues and cells. Importantly, LINC00668 expression was negatively correlated with miR-297 expression in OSCC tissues. Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Furthermore, LINC00668 knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67 in vivo. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling. In conclusion, these results suggest that LINC00668 promotes OSCC tumorigenesis via miR-297/VEGFA axis, which may provide a new target for the diagnosis and therapy of OSCC disease. - Highlights: • LINC00668 is up-regulated in human primary OSCC tissues. • Expression of VEGFA is up-regulated in primary human OSCC and negatively expressed related to miR-297. • miR-297 inhibits the tumorigenic potential of OSCC cells by down-regulating oncogenic VEGFA gene. • LINC00668's oncogenic functions are partially through reverse regulation of miRNA-297, and then activation of VEGFA.

60 APPLIED LIFE SCIENCES↗