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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 37 records · Page 2
All sourcesNASA NTRSDOE OSTI
DOE OSTI2020

Antibiotic tigecycline inhibits cell proliferation, migration and invasion via down‐regulating CCNE2 in pancreatic ductal adenocarcinoma

Abstract Recently, many researches have reported that antibiotic tigecycline has significant effect on cancer treatment. However, biomedical functions and molecular mechanisms of tigecycline in human pancreatic ductal adenocarcinoma (PDAC) remain unclear. In the current study, we tried to assess the effect of tigecycline in PDAC cells. AsPC‐1 and HPAC cells were treated with indicated concentrations of tigecycline for indicated time, and then, MTT, BrdU and soft agar assay were used to test cell proliferation. The effect of tigecycline on cell cycle and cellular apoptosis was tested by cytometry. Migration and invasion were detected by wound healing assay and transwell migration/invasion assay. Expressions of cell cycle‐related and migration/invasion‐related protein were determined by using Western blot. The results revealed that tigecycline observably suppressed cell proliferation by inducing cell cycle arrest at G0/G1 phase and blocked cell migration/invasion via holding back the epithelial‐mesenchymal transition (EMT) process in PDAC. In addition, tigecycline also remarkably blocked tumorigenecity in vivo. Furthermore, the effects of tigecycline alone or combined with gemcitabine in vitro or on PDAC xenografts were also performed. The results showed that tigecycline enhanced the chemosensitivity of PDAC cells to gemcitabine. Interestingly, we found CCNE2 expression was declined distinctly after tigecycline treatment. Then, CCNE2 was overexpressed to rescue tigecycline‐induced effect. The results showed that CCNE2 overexpression significantly rescued tigecycline‐inhibited cell proliferation and migration/invasion. Collectively, we showed that tigecycline inhibits cell proliferation, migration and invasion via down‐regulating CCNE2, and tigecycline might be used as a potential drug for PDAC treatment alone or combined with gemcitabine.

Yang, Jie↗
DOE OSTI2022

GIF Gas Cooled Fast Reactor: Proliferation Resistance and Physical Protection White Paper

This white paper represents the status of Proliferation Resistance and Physical Protection (PR&PP) characteristics for the Gas-cooled Fast reactor (GFR) reference designs selected by the Generation IV International Forum (GIF) GFR System Steering Committee (SSC). The intent is to generate preliminary information about the PR&PP features of the GFR reactor technology and to provide insights for optimizing their PR&PP performance for the benefit of GFR system designers. It updates the GFR analysis published in the 2011 report “Proliferation Resistance and Physical Protection of the Six Generation IV Nuclear Energy Systems”, prepared Jointly by the Proliferation Resistance and Physical Protection Working Group (PRPPWG) and the System Steering Committees and provisional System Steering Committees of the Generation IV International Forum, taking into account the evolution of both the systems, the GIF R&D activities, and an increased understanding of the PR&PP features. The white paper, prepared jointly by the GIF PRPPWG and the GIF GFR SSC, follows the high-level paradigm of the GIF PR&PP Evaluation Methodology to investigate the PR&PP features of the GIF GFR 2400 MWth reference design. The ALLEGRO reactor is also described. The EM2 and HEN MHR reactor are mentioned. An overview of fuel cycle for the GFR reference design and for the ALLEGRO reactor are provided. For PR, the document analyses and discusses the proliferation resistance aspects in terms of robustness against State-based threats associated with diversion of materials, misuse of facilities, breakout scenarios, and production in clandestine facilities. Similarly, for PP, the document discusses the robustness against theft of material and sabotage by non-State actors. The document follows a common template adopted by all the white papers in the updated series.

11 NUCLEAR FUEL CYCLE AND FUEL MATERIALS↗
DOE OSTI2021

EIF3H knockdown inhibits malignant melanoma through regulating cell proliferation, apoptosis and cell cycle

Highlights: • EIF3H is highly expressed in malignant melanoma and correlated with tumor stage and risk of lymphatic metastasis. • Knockdown of EIF3H inhibits cell proliferation, cell migration and promotes cell apoptosis of melanoma in vitro. • Knockdown of EIF3H suppresses tumor growth in vivo. Malignant melanoma (MM) causes 80% of skin cancer-related deaths and becomes the most lethal type of skin cancer. The molecular mechanism of MM is still not clear. This study aimed to reveal the relationship between MM and EIF3H. Clinical specimens were collected to preliminarily explore the role of EIF3H in MM. MM cell lines with EIF3H knockdown were constructed for investigating the effects of EIF3H on cell proliferation, apoptosis, cell cycle and cell motility. Mice xenograft model was constructed for verification in vivo. We found that EIF3H was obviously upregulated in MM tissues compared with normal skin tissues, which was correlated with tumor stage and risk of lymphatic metastasis. The in vitro results indicated that silencing EIF3H in MM cells could significantly suppress cell proliferation, promote cell apoptosis and induce cell cycle arrest. Moreover, EIF3H knockdown significantly restrained cell motility through regulating EMT-related proteins. The effects of EIF3H knockdown were also verified in mice xenograft model, which were represented by slower growth rate, smaller volume and lighter weight of tumors. Therefore, EIF3H was identified as a critical factor in the development and progression of MM which may be used as a novel therapeutic target in the treatment of MM.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

PCGF3 promotes the proliferation and migration of non-small cell lung cancer cells via the PI3K/AKT signaling pathway

Highlights: • PCGF3 is highly expressed in non-small cell lung cancer (NSCLC) tissues. • PCGF3 overexpression positively correlates with lymph node metastasis and p-TNM staging. • PCGF3 promotes NSCLC cells proliferation by regulating CyclinB1, CyclinD1, and CDK4. • PCGF3 promotes NSCLC cells migration by regulating RhoA, RhoC, and CDC42. • PCGF3 promotes malignant behavior in NSCLC by positively regulating the PI3K/AKT signaling pathway. The Polycomb Group Ring Finger 3 (PCGF3) protein has been reported to be significantly upregulated in pancreatic islet tumors and related to signal transduction; however, its detailed mechanisms and biological roles in other tumors, including non-small cell lung cancer (NSCLC), remain unclear. This study investigated the function of PCGF3 in NSCLC and further elucidated its mechanism of action. The immunohistochemical analysis of 86 selected lung cancer tissues revealed that PCGF3 was highly expressed in NSCLC tissues and positively correlated with lymph node metastasis and p-TNM staging. Additionally, PCGF3 promoted cell proliferation in lung cancer by regulating CyclinB1, CyclinD1, and CDK4 expression, and also promoting their migration by regulating RhoA, RhoC, and CDC42. Furthermore, PCGF3 affected both the proliferation and migration of lung cancer cells by regulating the PI3K/AKT pathway, as verified by inhibiting this pathway using LY294002. The findings of this study suggested that PCGF3 is associated with poor prognosis in patients with NSCLC and could therefore be an important biomarker for treating and preventing NSCLC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

The JmjC-domain protein NO66/RIOX-1 affects the balance between proliferation and maturation in acute myeloid leukemia

Highlights: • NO66/RIOX1 is not expressed in the AML cell line KG1a regarded as a “stem cell-like” model system. • NO66/RIOX1 is not expressed in primary HSC-enriched CD34{sup +}/CD38{sup -} cells of healthy donors. • Ectopic expression of NO66/RIOX1 in KG1a cells inhibits proliferation and rDNA transcription. • NO66/RIOX1 impacts on the transition from stem cells to progenitors by regulation of gene expression. As epigenetic regulators are frequently dysregulated in acute myeloid leukemia (AML) we determined expression levels of the JmjC-protein NO66 in AML cell lines and sub fractions of healthy human hematopoietic cells. NO66 is absent in the AML cell lines KG1/KG1a which consist of cells with the immature CD34{sup +}/CD38{sup -} phenotype and is regarded as a “stem cell-like” model system. Similarly, NO66 is not detectable in CD34{sup +}/CD38{sup -} cells purified from healthy donors but is clearly expressed in the more committed CD34{sup +}/CD38{sup +} cell population. Loss of NO66 expression in KG1/KG1a cells is due to hyper-methylation of its promoter and is released by DNA-methyltransferase inhibitors. In KG1a cells stably expressing exogenous wild type (KG1a66wt) or enzymatically inactive mutant (KG1a66mut) NO66, respectively, the wild type protein inhibited proliferation and rDNA transcription. Gene expression profiling revealed that the expression of NO66 induces a transcriptional program enriched for genes with roles in proliferation and maturation (e.g.EPDR1, FCER1A, CD247, MYCN, SNORD13). Genes important for the maintenance of stem cell properties are downregulated (e.g. SIRPA, Lin28B, JAML). Our results indicate that NO66 induces lineage commitment towards myeloid progenitor cell fate and suggest that NO66 contributes to loss of stem cell properties.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Ferredoxin reductase regulates proliferation, differentiation, cell cycle and lipogenesis but not apoptosis in SZ95 sebocytes

Highlights: • FDXR expression is increased in sebaceous cells of acne lesions. • FDXR may enhance sebocyte differentiation and lipogenesis via ROS production. • FDXR might inhibit proliferation through inducing G2/S blockade. • IGF-1 could facilitate sebaceous differentiation and lipogenesis via PI3K/Akt/FDXR pathway. Ferredoxin reductase (FDXR), a mitochondrial membrane-associated flavoprotein, is essential for electron transfer and modulates p53-dependent apoptosis in cancer cells.FDXR may be implicated in epidermal and sebocytic differentiation, but its explicit function in sebocytes remains to be elucidated. In the present study, immunohistochemistry revealed that FDXR expression was increased in sebaceous cells of acne lesions. FDXR, PPARγ, LXRα/β, SREBP1 and Sox9 expression was incremental during sebocyte differentiation. FDXR overexpression induced by Ad-GFP-FDXR infection enhanced differentiation, reactive oxygen species (ROS), lipogenesis and PPARγ expression, and consequnently inhibited proliferation in SZ95 sebocytes. Flow cytometry showed that FDXR overexpression induced significant blockade of G2/M phase but had no effect on sub-G1 (apoptotic) sebocytes. Insulin-like growth factor-1 (IGF-1)-induced FDXR and PPARγ expression and lipogenesis were abolished by pretreatment with PI3K inhibitor LY294002. These results suggest that FDXR overexpression might promote differentiation and lipogenesis via ROS production and suppress proliferation via G2/S blockade in SZ95 sebocytes. IGF-1 could facilitate differentiation and lipogenesis through PI3K/Akt/FDXR pathway. FDXR could serve as a potential marker of advanced sebaceous differentiation, and its overexpression may be involved in the development of acne lesions.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

RAN and YBX1 are required for cell proliferation and IL-4 expression and linked to poor prognosis in oral squamous cell carcinoma

Highlights: • RAN and YBX1 are co-expressed and required for cell proliferation in OSCC cells. • RAN and YBX1 are positively associated with the immune infiltrates of CD4{sup +} Th2 cells. • RAN and YBX1 can promote IL-4 expression. • RAN is a direct target of YBX1. • RAN and YBX1 can serve as potential co-biomarkers for poor prognosis in OSCC. Oral squamous cell carcinoma (OSCC) is one of the most common malignancies in the world, with a high mortality rate. RAN is a member of the Ras GTPase family and is overexpressed in a range of cancers, however, the relationship between RAN and OSCC is rarely reported. In this study, we found that RAN is overexpressed in OSCC tissues. RAN inhibition retarded OSCC cell proliferation and led to apoptosis and cell cycle arrest. Knockdown of RAN inhibited tumor growth in vivo. Strikingly, we found that RAN and oncogene Y-box binding protein-1 (YBX1) are positively associated with the immune infiltrates of CD4{sup +} Th2 cells in multiple types of cancer, and can promote IL-4 expression. IL-4 treatment can partially rescue RAN knockdown-induced cell apoptosis in OSCC cells. Moreover, overexpression of RAN could rescue cell growth inhibition caused by knockdown of YBX1. Furthermore, patients with low expression of both RAN and YBX1 had better overall survival than others. Collectively, these findings indicate that RAN is a target of YBX1. RAN and YBX1 are required for cell proliferation and IL-4 expression. RAN and YBX1 are co-expressed and can serve as potential co-biomarkers for poor prognosis in OSCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

MUSTN1 is an indispensable factor in the proliferation, differentiation and apoptosis of skeletal muscle satellite cells in chicken

The yield and quality of the skeletal muscle are important economic traits in livestock and poultry production. The musculoskeletal embryonic nuclear protein 1 (MUSTN1) gene has been shown to be associated with embryonic development, postnatal growth, bone and skeletal muscle regeneration; however, its function in the skeletal muscle development of chicken remains unclear. Therefore, in this study, we observed that the expression level of MUSTN1 increased in conjunction with the proliferation of chicken skeletal muscle satellite cells (SMSCs). Knockdown of MUSTN1 in SMSCs downregulated the expression of cell proliferation genes as Pax7, CDK-2 and differentiation-relate genes including MyoD, MyoG, MyHC and MyH1B, whereas it upregulates the expression of cell apoptosis gene (Caspase-3) (P < 0.05). However, the combined analysis of CCK-8 and EdU showed that the cell vitality and EdU-positive cells of the si-MUSTN1 transfected group were significantly lower than those of the negative siRNA group (P < 0.05). In addition, the knockdown of MUSTN1 significantly increased the cell population in the G0/G1 phase and significantly decreased the cell population in the G2/M phase (P < 0.05), whereas the overexpression of MUSTN1 showed opposite effect. Taken together, our findings indicates that MUSTN1 is an important molecular factor that is responsible for regulating muscle growth and development in chickens, particularly, proliferation and differentiation of SMSCs.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Necrosulfonamide reverses pyroptosis-induced inhibition of proliferation and differentiation of osteoblasts through the NLRP3/caspase-1/GSDMD pathway

The acute inflammatory stimulation occurring after a bone fracture regulates the repair and healing of local bone injury; however, under certain conditions, pyroptosis may occur in osteoblasts, which affects osteoblast proliferation and differentiation, thereby affecting the growth, development and morphological changes of bone tissue. The aim of the present study was to examine the effect of the pyroptosis inhibitor necrosulfonamide (NSA) on the proliferation and differentiation of osteoblasts and elucidate the underlying mechanism. The results revealed that NSA reversed the effects of ATP/lipopolysaccharide (LPS) on cell viability and pyroptosis, and on the mRNA and protein expression of pyroptosis-related genes. It also suppressed the secretion of IL-6, TNF-α and IL-1β and reversed the effects of ATP/LPS on the activity of ALP and the mRNA expression of differentiation-related genes in osteoblasts. The fact that overexpression of caspase-1, gasdermin D (GSDMD) and NLRP3 abolished the effects of NSA on the viability and pyroptosis of osteoblasts, as well as the mRNA expression of differentiation-related genes and the activity of ALP in osteoblasts, indicated that NSA promoted the proliferation and differentiation of osteoblasts by inhibiting the NLRP3/caspase-1/GSDMD pyroptosis pathway. The present study provides proof supporting the potential application of NSA for improving the function of osteoblasts in fracture repair and indicates the value of the NLRP3/caspase-1/GSDMD pyroptosis pathway as a pharmaceutical target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Sepsis induces muscle atrophy by inhibiting proliferation and promoting apoptosis via PLK1‐AKT signalling

Abstract Sepsis and sepsis‐induced skeletal muscle atrophy are common in patients in intensive care units with high mortality, while the mechanisms are controversial and complicated. In the present study, the atrophy of skeletal muscle was evaluated in sepsis mouse model as well as the apoptosis of muscle fibres. Sepsis induced atrophy of skeletal muscle and apoptosis of myofibres in vivo and in vitro. In cell‐based in vitro experiments, lipopolysaccharide (LPS) stimulation also inhibited the proliferation of myoblasts. At the molecular level, the expression of polo‐like kinase 1 (PLK1) and phosphorylated protein kinase B (p‐AKT) was decreased. Overexpression of PLK1 partly rescued LPS‐induced apoptosis, proliferation suppression and atrophy in C2C12 cells. Furthermore, inhibiting the AKT pathway deteriorated LPS‐induced atrophy in PLK1‐overexpressing C2C12 myotubes. PLK1 was found to participate in regulating apoptosis and E3 ubiquitin ligase activity in C2C12 cells. Taken together, these results indicate that sepsis induces skeletal muscle atrophy by promoting apoptosis of muscle fibres and inhibiting proliferation of myoblasts via regulation of the PLK1‐AKT pathway. These findings enhance understanding of the mechanism of sepsis‐induced skeletal muscle atrophy.

Cao, Ying‐Ya↗
DOE OSTI2023

Application of Proliferation Resistance Optimization (PRO-X) Methodology to a Generic Research Reactor

The Proliferation Resistance Optimization Program (PRO-X) has been established by the NNSA to provide a framework for evaluating and integrating proliferation resistance into nuclear reactor system (core, fuel, and auxiliary facilities) designs that also maintain the safety and peaceful use missions of those systems. The research reactor (PRO-RR) area is the component of PRO-X that supports the program objectives by applying state-of-the-art analysis methods to research reactor systems. This report details the results of using a defined set of analytical tools to evaluate the neutronics, thermal hydraulics and proliferation risk characteristics of a set of parametric cores based on a generic 10 MW materials test reactor that uses a plate-type low enriched uranium (LEU) fuel. The analysis shows that by suitable adjustment of the core size, reflector configuration and power level, mission performance and safety margins can be maintained or improved while reducing the potential for production of special nuclear material.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗
DOE OSTI2021

Artificial Judgement Assistance from teXt (AJAX): Applying Open Domain Question Answering to Nuclear Non-proliferation Analysis

Nuclear non-proliferation analysis is complex and subjective, as the data is sparse, and examples are rare and diverse. While analysing non-proliferation data, it is often desired that the findings be completely auditable such that any claim or assertion can be sourced directly to the reference material from which it was derived. Currently this is accomplished by analysts thoroughly documenting underlying assumptions and clearly referencing details to source documents. This is a labour-intensive and time-consuming process that can be difficult to scale with geometrically increasing quantities of data. In this work, we describe an approach to leverage bi-directional language models for nuclear non-proliferation analysis. It has been shown recently that these models not only capture language syntax but also some of the relational knowledge present in the training data. We have devised a unique Salt and Pepper strategy for testing the knowledge present in the language models, while also introducing auditability function in our pipeline. We demonstrate that fine-tuning the bi-directional language models on domain specific corpus improves their ability to answer domain-specific factoid questions. Our hope is that the results presented in this paper will further the natural language processing (NLP) field by introducing the ability to audit the answers provided by the language models to bring forward the source of said knowledge.

98 NUCLEAR DISARMAMENT, SAFEGUARDS, AND PHYSICAL P↗
DOE OSTI2021

miR-31-5p promotes proliferation and inhibits apoptosis of goat hair follicle stem cells by targeting RASA1/MAP3K1 pathway

Highlights: • MAP3K1 was upregulated in hair follicle stem cells in response to overexpression miR-31–5p. • We confirmed RASA1 as a target gene of miR-31–5p. • Inhibition of miR-31–5p promotes apoptosis. • The miR-31–5p/RASA1/MAP3K1 axis regulates hair follicle stem cells activity via MAPK pathway. The Yangtze River Delta white goat is a sole goat species that can naturally produce superior-quality brush hair. It's worth to mention that study the developmental mechanism of goat hair follicle stem cells is vital for future breed preservation and molecular breeding. In this study, we successfully isolated hair follicle stem cells from the skin tissue of fetal sheep neck spine, and harvested superior-quality and normal-quality brush hair goat tissue. The expression of miR-31-5p in goat hair follicle stem cells was verified by qPCR and Western blot. The effects of overexpression or inhibition of miR-31-5p on the proliferation and apoptosis of hair follicle stem cells were detected by EdU, CCK-8, flow cytometry, etc. miR-31-5p can significantly improve cell proliferation and inhibit cell apoptosis by targeting RASA1 and upregulating MAP3K1 level, whereas miR-31-5p knockdown led to an opposite effect. These results reveal a miR-31-5p-associated regulatory network between miR-31-5p and RASA1/MAP3K1 during the progression of superiorquality brush hair traits.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Knockdown of DDX46 suppresses the proliferation and invasion of gastric cancer through inactivating Akt/GSK-3β/β-catenin pathway

DEAD-box RNA helicase 46 (DDX46) has recently been identified as a candidate oncogene in several types of human malignancies. To date, the role of DDX46 in gastric cancer has not been determined. The purpose of the current study was to explore the role of DDX46 in gastric cancer and the potential mechanism. DDX46-silecing or overexpressing gastric cancer cell lines were established to validate the role of DDX46. Our results showed that the expression of DDX46 was significantly increased in gastric cancer tissues and cell lines. Knockdown of DDX46 suppressed the proliferation and invasion of gastric cancer cells. Whereas, DDX46 overexpression enhanced the cell proliferation and invasion of gastric cancer cells. Furthermore, knockdown of DDX46 markedly suppressed the tumor growth of xenografts. Research into the mechanism revealed that DDX46 depletion inhibited the Akt/GSK-3β/β-catenin signaling pathway in gastric cancer cells. Notably, activation of Akt or β-catenin overexpression reversed the DDX46 depletion-mediated anti-cancer effect. In conclusion, these findings indicated that DDX46 exerted an oncogenic role in gastric cancer via regulating the Akt/GSK-3β/β-catenin signaling pathway. Thus, DDX46 might be utilized as a therapeutic anti-cancer target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

LncRNA DLEU2 promotes cervical cancer cell proliferation by regulating cell cycle and NOTCH pathway

Highlights: • LncRNA DLEU2 is upregulated and related to tumor topography in cervical cancer. • LncRNA DLEU2 promotes cervical cancer cell proliferation. • LncRNA DLEU2 promotes the progression of the cell cycle. • LncRNA DLEU2 inhibits the activity of the Notch signaling pathway. Long noncoding RNAs (lncRNAs) are known to play a crucial role in the onset and progression of cervical cancer (CC). Here, the results of RNA microarray and RNA-sequencing dataset analysis showed that lncRNA DLEU2 was significantly upregulated in CC tissues. Clinicopathologic analysis indicated that lncRNA DLEU2 was closely related to tumor topography. Functional experiments and bioinformatics analysis revealed that lncRNA DLEU2 promoted CC cell proliferation and accelerated the cell cycle. Mechanistically, lncRNA DLEU2 promoted the progression of the cell cycle and inhibited the activity of the Notch signaling pathway by inhibiting p53 expression. Additionally, lncRNA DLEU2 probably interacted with ZFP36 Ring Finger Protein (ZFP36) to inhibit the expression of p53. In conclusion, this study revealed the function of lncRNA DLEU2 in CC tumorigenesis, suggesting new therapeutic targets in CC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Targeting HSPA8 inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity in imatinib-resistant chronic myeloid leukemia cells

The resistance to tyrosine kinase inhibitors is currently a major problem for chronic myeloid leukemia (CML) treatment and HSPA8 is highly expressed and a hallmark of poor prognosis in several human cancers. However, its role in imatinib-resistant CML (IR-CML) cells remains undetermined. Here, we determined HSPA8 was overexpressed in IR-CML cells and associated with imatinib resistance. HSPA8 ablation could downregulate BCR-ABL/STAT5 and BCR-ABL/AKT signaling pathways, dramatically induce proliferation inhibition, autophagy, G0/G1 phase cell cycle arrest but not apoptosis in IR-CML cells. Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo. These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

PDRG1 predicts a poor prognosis and facilitates the proliferation and metastasis of colorectal cancer

Highlights: • PDRG1 is overexpressed in colorectal cancer tissues and is associated with poor prognosis of colorectal cancer patients. • PDRG1 regulates the proliferation, apoptosis, cell cycle progression and metastasis of colorectal cancer cells. • PDRG1 promotes the proliferation, migration and invasion of colorectal cancer via p21-mediated cell cycle progression. The incidence and mortality of colorectal cancer (CRC) is increasing yearly and CRC patients are becoming younger in global. Evidences have revealed the carcinogenic effect of p53 and DNA damage-regulated gene 1 (PDRG1) in several types of tumors. However, its biological function is yet to be investigated in CRC. This study aimed to unveil the prooncogenic role of PDRG1 in CRC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2023

Twin Proliferation and Prolongation under Kinetic Control: Pd–Au Janus Icosahedra versus Pd@Au Core–Shell Starfishes

Heterogeneous bimetallic nanocrystals featuring explicit spatial configurations and abundant twin defects can simultaneously enable geometric and ligand effects to enhance catalytic and photonic applications. Herein, we report two growth patterns of Au atoms on penta-twinned Pd decahedra, involving twin proliferation to generate asymmetric Pd–Au Janus icosahedra and twin elongation to produce anisotropic Pd@Au core–shell starfishes, respectively. Mechanistic analysis indicates that the injection rate determines the lower-limit number (n low ) of Au(III) ions in the steady state and thus controls the growth pattern. When n low ≤ 5.5, the kinetic rate is slow enough to initiate asymmetrical one-side growth but fast enough to outpace surface diffusion; Au tetrahedral subunits are successively proliferated along the axial $\langle$110$\rangle$ direction of Pd decahedra to form Pd–Au Janus icosahedra. Composed of five Pd and 15 Au tetrahedral subunits, such a heterogeneous icosahedron supports high (2.2 GPa) tensile strain and high strain difference up to +21.9%. In contrast, when n low > 5.5, the fast reduction kinetics promotes symmetric growth with inadequate surface diffusion. As such, Au atoms are laterally deposited along five high-indexed $\langle$211$\rangle$ ridges of Pd decahedra to generate concave Pd@Au core–shell starfishes with tunable sizes (28–40 nm), twin elongation ratios (33.82–162.08%), and lattice expansion ratios (8.82–20.10%).

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗