Bioaccumulation of polycyclic aromatic hydrocarbons and their human health risks depend on the characteristics of microplastics in marine organisms of Sanggou Bay, China.

Microplastics pose a threat to marine environments through their physical presence and as vectors of chemical pollutants. However, the impact of microplastics on the accumulation and human health risk of chemical pollutants in marine organisms remains largely unknown. In this study, we investigated the microplastics and polycyclic aromatic hydrocarbons (PAHs) pollution in marine organisms from Sanggou Bay and analyzed their correlations. Results showed that microplastic and PAHs concentration ranged from 1.23 ± 0.23 to 5.77 ± 1.10 items/g, from 6.98 ± 0.45 to 15.07 ± 1.25 µg/kg, respectively. The microplastic abundance, particularly of fibers, transparent and color plastic debris, correlates strongly with PAH contents, indicating that microplastics increase the bioaccumulation of PAHs and microplastics with these characteristics have a significant vector effect on PAHs. Although consuming seafood from Sanggou Bay induce no carcinogenic risk from PAHs, the presence of microplastics in organisms can significantly increases incremental lifetime cancer risk of PAHs. Thus, microplastics can serve as transport vectors for PAHs with implications for the potential health risks to human through consumption. This study provides new insight into the risks of microplastics in marine environments.

Inhibitory mechanisms of decoy receptor 3 in cecal ligation and puncture-induced sepsis.

Despite its high mortality, specific and effective drugs for sepsis are lacking. Decoy receptor 3 (DcR3) is a potential biomarker for the progression of inflammatory diseases. The recombinant human DcR3-Fc chimera protein (DcR3.Fc) suppresses inflammatory responses in mice with sepsis, which is critical for improving survival. The Fc region can exert detrimental effects on the patient, and endogenous peptides are highly conducive to clinical application. However, the mechanisms underlying the effects of DcR3 on sepsis are unknown. Herein, we aimed to demonstrate that DcR3 may be beneficial in treating sepsis and investigated its mechanism of action. Recombinant DcR3 was obtained in vitro. Postoperative DcR3 treatment was performed in mouse models of lipopolysaccharide- and cecal ligation and puncture (CLP)-induced sepsis, and their underlying molecular mechanisms were explored. DcR3 inhibited sustained excessive inflammation in vitro, increased the survival rate, reduced the proinflammatory cytokine levels, changed the circulating immune cell composition, regulated the gut microbiota, and induced short-chain fatty acid synthesis in vivo. Thus, DcR3 protects against CLP-induced sepsis by inhibiting the inflammatory response and apoptosis. Our study provides valuable insights into the molecular mechanisms associated with the protective effects of DcR3 against sepsis, paving the way for future clinical studies. IMPORTANCE: Sepsis affects millions of hospitalized patients worldwide each year, but there are no sepsis-specific drugs, which makes sepsis therapies urgently needed. Suppression of excessive inflammatory responses is important for improving the survival of patients with sepsis. Our results demonstrate that DcR3 ameliorates sepsis in mice by attenuating systematic inflammation and modulating gut microbiota, and unveil the molecular mechanism underlying its anti-inflammatory effect.

Unveiling the Role of Protein Kinase C θ in Porcine Epidemic Diarrhea Virus Replication: Insights from Genome-Wide CRISPR/Cas9 Library Screening.

Porcine epidemic diarrhea virus (PEDV), a member of the Alpha-coronavirus genus in the Coronaviridae family, induces acute diarrhea, vomiting, and dehydration in neonatal piglets. This study aimed to investigate the genetic dependencies of PEDV and identify potential therapeutic targets by using a single-guide RNA (sgRNA) lentiviral library to screen host factors required for PEDV infection. Protein kinase C θ (PKCθ), a calcium-independent member of the PKC family localized in the cell membrane, was found to be a crucial host factor in PEDV infection. The investigation of PEDV infection was limited in Vero and porcine epithelial cell-jejunum 2 (IPEC-J2) due to defective interferon production in Vero and the poor replication of PEDV in IPEC-J2. Therefore, identifying suitable cells for PEDV investigation is crucial. The findings of this study reveal that human embryonic kidney (HEK) 293T and L929 cells, but not Vero and IPEC-J2 cells, were suitable for investigating PEDV infection. PKCθ played a significant role in endocytosis and the replication of PEDV, and PEDV regulated the expression and phosphorylation of PKCθ. Apoptosis was found to be involved in PEDV replication, as the virus activated the PKCθ-B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) axis in HEK293T and L929 cells to increase viral endocytosis and replication via mitochondrial apoptosis. This study demonstrated the suitability of HEK293T and L929 cells for investigating PEDV infection and identified PKCθ as a host factor essential for PEDV infection. These findings provide valuable insights for the development of strategies and drug targets for PEDV infection.

Significance of the cGAS-STING Pathway in Health and Disease.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a significant role in health and disease. In this pathway, cGAS, one of the major cytosolic DNA sensors in mammalian cells, regulates innate immunity and the STING-dependent production of pro-inflammatory cytokines, including type-I interferon. Moreover, the cGAS-STING pathway is integral to other cellular processes, such as cell death, cell senescence, and autophagy. Activation of the cGAS-STING pathway by "self" DNA is also attributed to various infectious diseases and autoimmune or inflammatory conditions. In addition, the cGAS-STING pathway activation functions as a link between innate and adaptive immunity, leading to the inhibition or facilitation of tumorigenesis; therefore, research targeting this pathway can provide novel clues for clinical applications to treat infectious, inflammatory, and autoimmune diseases and even cancer. In this review, we focus on the cGAS-STING pathway and its corresponding cellular and molecular mechanisms in health and disease.

Dietary resveratrol supplementation on growth performance, immune function and intestinal barrier function in broilers challenged with lipopolysaccharide.

This study discusses the effects of resveratrol (RES) on the productive performance, immune function and intestinal barrier function of broiler chickens challenged with lipopolysaccharide (LPS). Two hundred and forty 1-day-old male Arbor Acres broilers were randomly divided into 4 groups of 6 replicates each, with 10 broilers per replicate. This experiment used a 2 × 2 factorial design with dietary factors (basal diets or basal diets supplemented with 400 mg/kg RES were administered from d 1 to 21) and stress factors (intraperitoneal injection of 0.5 mg/kg BW of saline or LPS at 16, 18 and 20 d of age). The results showed that LPS challenge had a significant adverse effect on average daily gain (ADG) in broilers at 16 to 21 d of age (P < 0.05), whereas the addition of RES to the diet inhibited the LPS-induced decrease in ADG (P < 0.05). RES also alleviated LPS-induced immune function damage in broilers, which was manifested by the decrease of spleen index (P < 0.05) and the recovery of serum immunoglobulin M and ileal secretory immunoglobulin A content (P < 0.05). The LPS challenge also disrupts intestinal barrier function and inflammation, and RES mitigates these adverse effects in different ways. RES attenuated LPS-induced reduction of villus height in the jejunum and ileum of broilers (P < 0.05). LPS also caused an abnormal increase in plasma D-lactic acid levels in broilers (P < 0.05), which was effectively mitigated by RES (P < 0.05). LPS challenge resulted in a significant decrease in mRNA expression of occludin in the intestinal mucosa (P < 0.05), which was mitigated by the addition of RES (P < 0.05). RES significantly decreased the mRNA expression of toll-like receptor 4, nuclear factor kappa-B and tumor necrosis factor alpha in the ileum tissue stimulated by LPS (P < 0.05). Taken together, this study shows that RES exerts its beneficial effect on broilers challenged with LPS by alleviating immune function damage, relieving intestinal inflammation and barrier damage, and thus improving growth performance.

The Dilemma of HSV-1 Oncolytic Virus Delivery: The Method Choice and Hurdles.

Oncolytic viruses (OVs) have emerged as effective gene therapy and immunotherapy drugs. As an important gene delivery platform, the integration of exogenous genes into OVs has become a novel path for the advancement of OV therapy, while the herpes simplex virus type 1 (HSV-1) is the most commonly used. However, the current mode of administration of HSV-1 oncolytic virus is mainly based on the tumor in situ injection, which limits the application of such OV drugs to a certain extent. Intravenous administration offers a solution to the systemic distribution of OV drugs but is ambiguous in terms of efficacy and safety. The main reason is the synergistic role of innate and adaptive immunity of the immune system in the response against the HSV-1 oncolytic virus, which is rapidly cleared by the body's immune system before it reaches the tumor, a process that is accompanied by side effects. This article reviews different administration methods of HSV-1 oncolytic virus in the process of tumor treatment, especially the research progress in intravenous administration. It also discusses immune constraints and solutions of intravenous administration with the intent to provide new insights into HSV-1 delivery for OV therapy.

Endoluminal Vacuum-Assisted Closure Therapy for Upper Gastrointestinal Leak, Perforation, and Fistula: A Case Series and Literature Review.

BACKGROUND: With the increasing incidence of upper digestive tract tumors, more upper digestive tract surgeries are performed each year, and surgeons have difficulty in the postoperative management of gastrointestinal anastomotic fistula. The use of a new minimally invasive technique, endoluminal vacuum-assisted closure (E-VAC), has increased the success rate of the treatment of gastrointestinal fistula. METHODS: We present 6 cases of gastrointestinal fistula treated in our hospital in 2021: 3 cases of anastomotic fistula after esophageal cancer surgery, 2 cases of anastomotic fistula after gastric cancer surgery, and one case of esophageal rupture after trauma. With E-VAC and other adjuvant treatment measures, the gastrointestinal fistulas were eventually closed or significantly reduced. RESULTS: Both local and systemic infections in all 6 patients were controlled with the use of E-VAC device, resulting in significant reduction or closure of fistulas. CONCLUSION: E-VAC devices can effectively help in the removal of the exudate and necrotic tissue around the fistula, promote the proliferation of granulation tissue, and support closure of the fistula. However, further improvements to the device are needed to improve patient comfort and operational safety.

Kombucha ameliorates LPS-induced sepsis in a mouse model.

As a popular traditional fermented beverage, kombucha has been extensively studied for its health benefits. However, the science behind the anti-inflammatory effect of kombucha has not been well studied, and there is an urgent need to uncover the secrets of the anti-inflammatory properties of kombucha. Here, we investigate kombucha's protective effects against lipopolysaccharide (LPS)-induced sepsis and on the intestinal microecology in mice. The contents of reducing sugars, polyphenols, catechins, and organic acids in the kombucha group were identified using various methods. The results showed that the concentrations of acetic acid, gluconic acid, polyphenol, and glucuronic acid in the kombucha group were 55.70 ± 2.57 g L-1, 50.20 ± 1.92 g L-1, 2.36 ± 0.31, and 1.39 ± 0.22 g L-1, respectively. The result also demonstrated that kombucha effectively improves the survival rate from 0% to 40%, and increases the thermoregulation in LPS-treated mice, which showed decreased mobility and had lost their appetite for food. Furthermore, kombucha reduced the levels of tumor necrosis factor-α and interleukins (IL)-1ß and IL-6, restored the levels of T cells and macrophages in LPS-challenged mice, alleviated the histopathological damage, and inhibited NF-κB signaling in mice with LPS-induced sepsis. We demonstrated that kombucha effectively prevents cellular immune function disorder in mice at the initial stage of sepsis and exerts an immunomodulatory effect. In addition, the effect of kombucha on the gut microbiota was investigated during sepsis. Kombucha supplementation altered the diversity of the gut microbiota and promoted the growth of butyrate-producing bacteria, which exert anti-inflammatory effects. Our results illustrate the potential of kombucha as a novel anti-inflammatory agent against the development of systemic inflammatory responses associated with sepsis.

High-speed giant magnetostrictive actuator using laminated silicon steel core.

The high-frequency eddy current loss limits the output speed of the giant magnetostrictive actuator (GMA). This paper investigates a GMA using a laminated silicon steel core. Compared with the integral silicon steel core, the laminated silicon steel core can reduce the equivalent conductivity and eddy currents. The laminated structure reduces the magnetic reluctance of the core and increases the magnetic field intensity in the giant magnetostrictive material rod. Therefore, the actuator can output large vibration amplitude under high-frequency magnetic field. At the sinusoidal excitation current of 35 A (rms) @ 2 kHz, the output vibration amplitude of the actuator using the laminated silicon steel core is 11.1 µm @ 4 kHz, which is 44.2% higher than that of the actuator with the integral silicon steel core. This indicates that the laminated structure of the magnetic core is beneficial to improve the output speed of GMA.

Associations of MTA1 expression with CT features, pathology and prognosis of elderly patients with non-small cell lung cancer.

Associations of metastasis-associated protein 1 (MTA1) expression with computed tomography (CT) features, pathology and prognosis of elderly patients with non-small cell lung cancer (NSCLC), and its clinical significance were explored. A total of 98 elderly patients with NSCLC were selected and underwent CT examination. The expression of MTA1 in carcinoma tissues and para-carcinoma normal tissues was detected via immunohistochemistry, and its associations with CT features, pathology and prognosis were analyzed. The results manifested that the expression of MTA1 in carcinoma tissues was significantly higher than that in para-carcinoma normal tissues, and it was associated with the degree of differentiation, stage and lymph node metastasis (P<0.05). Besides, the high expression of MTA1 was also related to the spicule sign, pleural indentation and lymph node metastasis (P<0.05) as well as the CT perfusion parameter capillary permeability (PMB) (P<0.05), but not to blood volume (BV), blood flow (BF) or time to peak (TTP). Moreover, the patients with high expression of MTA1 had significantly shorter survival time and a remarkably lower 5-year survival rate than those with low expression of MTA1 (P<0.05). In conclusion, MTA1 plays a certain role in the occurrence and development of NSCLC in elderly patients and has an association with their prognosis, which can provide references for the treatment and prognosis of NSCLC, with important clinical significance.

Microplastics in the commercial seaweed nori.

Microplastics have been reported to attach to the marine macroalgae which act as the vector for microplastic transfer in the marine food web. In this study, the edible seaweed nori (Pyropia spp.) was chosen as a target species. The microplastic contaminant situations in nori were analyzed in both its final commercial products and the intermediate products across different processing stages. The abundance of microplastics ranged from 0.9 to 3.0 items/g (dw) among 24 brands of commercially packaged nori samples. With the development of nori processing stages, an enlarged size fraction of greater microplastics (1-5 mm) was observed. Compared with commercially packaged nori samples, the proportions of polypropylene, polyethylene and poly (ethylene-propylene) copolymers increased, whereas that of polyester decreased in factory-processed nori. Additionally, we further simulated and quantified the number of fluorescent polyester fibers (concentrations: 0, 1000, 5000, 10,000 fibers/L) attach to the algal pieces of Pyropia yezoensis under laboratory conditions. The average abundance of microfibers on the nori was positively and quantitatively related to their abundances in seawater (p < 0.01). To our best knowledge, this is the first work that shows the prevalence of microplastics in the commercial seaweed nori and relates to their potential sources during the processing phase.

Coix seed improves growth performance and productivity in post-weaning pigs by reducing gut pH and modulating gut microbiota.

Coix seed has traditionally been used in traditional Chinese medicine to fortify the spleen and inhibit dampness, and has shown anticancer effects in humans. However, it is not known whether coix seed improves post-weaning growth performance and productivity, and the mechanism of interaction between coix seed and gut microbiota remains unknown. In this study, we established four groups: (i) control, (ii) antibiotic-fed, (iii) coix seed powder-fed, and (iv) coix seed extract-fed. The feeding experiment was conducted for 4 weeks. Coix seed extract significantly increased average weight gain and reduced the feed/meat ratio in weaned pigs, in addition to reducing the pH of their gastric juice. Further assays demonstrated that coix seed promotes an increase in the density and length of the gastrointestinal villi. Next, 16s sequencing of gut microbiota showed that coix seed significantly increased the abundance of phylum Bacteroidetes and genus Lactobacillus (p < 0.05) and reduced the abundance of phylum Prevotella (p < 0.05) in the gut microbiota. In contrast, the abundance of phylum Bacteroidetes and genus Lactobacillus decreased in the control group and antibiotic group, whereas the abundance of phylum Prevotella increased. Our findings indicate that coix seed improves growth performance and productivity in post-weaning pigs by reducing the pH value of gastric juice, increasing the density and length of gastrointestinal villi, and modulating gut microbiota. Thus, coix seed has good potential for use as a feed supplement in swine production.

Rescue of a Mouse Model of Spinal Muscular Atrophy With Respiratory Distress Type 1 by AAV9-IGHMBP2 Is Dose Dependent.

Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is an autosomal recessive disease occurring during childhood. The gene responsible for disease development is a ubiquitously expressed protein, IGHMBP2. Mutations in IGHMBP2 result in the loss of α-motor neurons leading to muscle atrophy in the distal limbs accompanied by respiratory complications. Although genetically and clinically distinct, proximal SMA is also caused by the loss of a ubiquitously expressed gene (SMN). Significant preclinical success has been achieved in proximal SMA using viral-based gene replacement strategies. We leveraged the technologies employed in SMA to demonstrate gene replacement efficacy in an SMARD1 animal model. Intracerebroventricular (ICV) injection of single-stranded AAV9 expressing the full-length cDNA of IGHMBP2 in a low dose led to a significant level of rescue in treated SMARD1 animals. Consistent with drastically increased survival, weight gain, and strength, the rescued animals demonstrated a significant improvement in muscle, NMJ, motor neurons, and axonal pathology. In addition, increased levels of IGHMBP2 in lumbar motor neurons verified the efficacy of the virus to transduce the target tissues. Our results indicate that AAV9-based gene replacement is a viable strategy for SMARD1, although dosing effects and potential negative impacts of high dose and ICV injection should be thoroughly investigated.

Pharmacologically induced mouse model of adult spinal muscular atrophy to evaluate effectiveness of therapeutics after disease onset.

Spinal muscular atrophy (SMA) is a genetic disease characterized by atrophy of muscle and loss of spinal motor neurons. SMA is caused by deletion or mutation of the survival motor neuron 1 (SMN1) gene, and the nearly identical SMN2 gene fails to generate adequate levels of functional SMN protein due to a splicing defect. Currently, several therapeutics targeted to increase SMN protein are in clinical trials. An outstanding issue in the field is whether initiating treatment in symptomatic older patients would confer a therapeutic benefit, an important consideration as the majority of patients with milder forms of SMA are diagnosed at an older age. An SMA mouse model that recapitulates the disease phenotype observed in adolescent and adult SMA patients is needed to address this important question. We demonstrate here that Δ7 mice, a model of severe SMA, treated with a suboptimal dose of an SMN2 splicing modifier show increased SMN protein, survive into adulthood and display SMA disease-relevant pathologies. Increasing the dose of the splicing modifier after the disease symptoms are apparent further mitigates SMA histopathological features in suboptimally dosed adult Δ7 mice. In addition, inhibiting myostatin using intramuscular injection of AAV1-follistatin ameliorates muscle atrophy in suboptimally dosed Δ7 mice. Taken together, we have developed a new murine model of symptomatic SMA in adolescents and adult mice that is induced pharmacologically from a more severe model and demonstrated efficacy of both SMN2 splicing modifiers and a myostatin inhibitor in mice at later disease stages.

Astrocytes influence the severity of spinal muscular atrophy.

Systemically low levels of survival motor neuron-1 (SMN1) protein cause spinal muscular atrophy (SMA). α-Motor neurons of the spinal cord are considered particularly vulnerable in this genetic disorder and their dysfunction and loss cause progressive muscle weakness, paralysis and eventually premature death of afflicted individuals. Historically, SMA was therefore considered a motor neuron-autonomous disease. However, depletion of SMN in motor neurons of normal mice elicited only a very mild phenotype. Conversely, restoration of SMN to motor neurons in an SMA mouse model had only modest effects on the SMA phenotype and survival. Collectively, these results suggested that additional cell types contribute to the pathogenesis of SMA, and understanding the non-autonomous requirements is crucial for developing effective therapies. Astrocytes are critical for regulating synapse formation and function as well as metabolic support for neurons. We hypothesized that astrocyte functions are disrupted in SMA, exacerbating disease progression. Using viral-based restoration of SMN specifically to astrocytes, survival in severe and intermediate SMA mice was observed. In addition, neuromuscular circuitry was improved. Astrogliosis was prominent in end-stage SMA mice and in post-mortem patient spinal cords. Increased expression of proinflammatory cytokines was partially normalized in treated mice, suggesting that astrocytes contribute to the pathogenesis of SMA.

Diol glycidyl ether-bridged cyclens: preparation and their applications in gene delivery.

Polymeric 1,4,7,10-tetraazacyclododecanes (cyclens) using diol glycidyl ether with different chain length as bridges (5a-e) were designed and synthesized from various diols, 1,7-diprotected cyclen and epichlorohydrin. The molecular weights of the title polymers were measured by GPC with good polydispersity. Agarose gel retardation and fluorescent titration using ethidium bromide showed good DNA-binding ability of 5. They could retard plasmid DNA (pDNA) at an N/P ratio of 4-6 and form polyplexes with sizes around 100-250 nm from an N/P ratio of 10 to 60 and relatively low zeta-potential values (5-22 mV). The cytotoxicity of 5 assayed by MTT is much lower than that of 20 kDa PEI. In vitro transfection against A549 and 293 cells showed that the transfection efficiency (TE) of 5c/DNA polyplexes is close to that of 20 kDa PEI at an N/P ratio of 5. Structure-activity relationship (SAR) of 5 was discussed in their DNA-binding, cytotoxicity, and transfection studies. The TE of 5c/DNA polyplexes could be improved by the introduction of 50 µM of chloroquine, the endosomolytic agents, to pretreated cells. These studies may extend the application areas of macrocyclic polyamines, especially for cyclen.

[Study on characterization of the complexes of FUS1/hIL-12 with cationic liposome].

This study was aimed to shed light on the biological and pharmaceutical characterization of the complexes of FUS1/hIL-12 double gene with cationic liposome, and to assess such complexes' transfection efficiency, stability and cytotoxicity; for they have the potential for use as drugs in gene therapy of lung cancer. Gel retardation assay, diameter measurement, and surface charge by photon correlation spectroscopy (PCS) were employed to select the appropriate ratio of "cationic liposome to DNA" of the double-gene and liposome complexes. The plasmid EGFP and plasmid PVITO2-hIL12-FUS1 mediated by cationic liposome were transfected into A549 lung cancer cells respectively, and the expression levels of EGFP and FUS1 and hIL-12 were determined by inverted fluorescence microscope and immunohistochemical and enzyme linked immunosorbent assay (ELISA) respectively. Agarose gel electrophoresis was performed to detect the stability of the double-gene and liposome complexes, after they were incubated with serum and Dnase I respectively. After the erythrocytes being incubated with the complexes of FUS1/hIL-12 with cationic liposome, the morphology of erythrocyte was observed by microscopy. The result of this study provides a basis for the use of the complexes of FUS1/hIL-12 with cationic liposome in gene therapy of lung cancer.

Linear cyclen-based polyamine as a novel and efficient reagent in gene delivery.

Linear cyclen-based polyamine (LCPA, M(w) = 7392, M(w)/M(n) = 1.19) as a novel non-viral gene vector was designed and synthesized from 1,7-diprotected 1,4,7,10-tetraazacyclododecane (cyclen), bis(beta-hydroxylethyl)amine and epichlorohydrin. Agarose gel retardation and fluorescent titration using ethidium bromide showed the good DNA-binding ability of LCPA. It could retard pDNA at an N/P ratio of 4 and form polyplexes with sizes around 250-300 nm from an N/P ratio of 10 to 60 and relatively lower zeta-potential values (< +3 mV) even at the N/P ratio of 60. The cytotoxicity of LCPA assayed by MTT is much lower than that of 25 kDa PEI. In vitro transfection against A549 and 293 cells showed that the transfection efficiency of LCPA/DNA polyplexes is close to that of 25 kDa PEI at an N/P ratio of 10-15, indicating that the new material could be a promising non-viral polycationic reagent for gene delivery.

[Study on invasion and metastasis-associated genes of lung cancer related with NM23-H1 gene].

OBJECTIVE: To study on invasion and metastasis-associated genes of lung cancer related with NM23-H1 gene. METHODS: Human gene expression chip based on the subtracted cDNA libraries was constructed. After microarray hybridization, clones sequencing, sequence homology search, the information of differently expressed genes in human large cell lung cancer cell line of L9981 and L9981-nm23-H1 were obtained and then further confirmed by real-time quantitative PCR. RESULTS: Gene expression profiling chips of differently expressed genes in human large cell lung cancer cell line L9981 and L9981-nm23-H1 were successfully constructed. After microarray hybridization, sequence homology search, 19 differentially expressed genes were observed. After real-time quantitative PCR evaluation, we found that the mRNA of 8 genes including PSMA7, SBDS, ODC1, YARS, CSDA, PTP4A1, SHPRH and TOMM7 was up-regulated in the cell line of L9981 after transfected with NM23-H1 gene, whereas the mRNA of PKM2 and GMNN was down-regulated. CONCLUSION: NM23-H1 gene may be the upstream regulator of metastasis-associated genes, which can regulate the downstream genes to achieve a series of lung cancer metastatic potential.