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Fei Su

Publications and source records attributed to Fei Su.

12 recordsLinked to original sources
PubMed2025

KLF5 facilitates lung adenocarcinoma metastasis by regulating the epithelial-mesenchymal transition pathway through RHPN2.

BACKGROUND: Distant metastasis is a primary factor contributing to the significantly shorter survival time of patients with advanced lung adenocarcinoma. The transcription factor Kruppel-like factor 5 (KLF5) facilitates the progression of lung adenocarcinoma. However, the specific mechanism by which KLF5 is involved in the tumor metastasis of lung adenocarcinoma metastasis remains largely unclear. METHODS: Using bioinformatic analysis, Rhophilin Rho GTPase Binding Protein 2 (RHPN2) was identified as a potential downstream target gene for KLF5; it plays a crucial role in the regulation of the epithelial-mesenchymal transformation pathway in lung adenocarcinoma. Western blotting and immunohistochemistry were performed to examine RHPN2 expression in lung adenocarcinoma. In vivo and in vitro experiments were conducted to explore the regulatory role of RHPN2 on the cell growth and metastasis of lung adenocarcinoma. Chromatin immunoprecipitation sequencing was used to analyze the direct binding activity between KLF5 and RHPN2 promoter regions. Luciferase activity assay was performed to verify the transcriptional activation effect of KLF5 on RHPH2. RESULTS: RHPN2 was highly expressed in lung adenocarcinoma; patients with lung adenocarcinoma who showed high RHPN2 expression had a poor prognosis. In vivo and in vitro experiments showed that RHPN2 promoted cell growth and metastasis and activated the epithelial-mesenchymal transformation pathway in lung adenocarcinoma. KLF5 directly bound to the promoter region of RHPN2 and upregulated its expression in lung adenocarcinoma through transcriptional activation. In addition, rescue experiments confirmed that KLF5 facilitated the progression of lung adenocarcinoma in an RHPN2-dependent manner. CONCLUSION: Our study offers insights into the potential mechanisms of metastasis in lung adenocarcinoma and highlights RHPN2 as a potential therapeutic target.

Humans↗
PubMed2006

Experimental study on denitrification using coated electrode of immobilized denitrifying bacteria.

OBJECTIVE: To develop a coated electrode of immobilized denitrificants and to evaluate the performance of a bioelectrochemical reactor to enhance and control denitrification. METHODS: Denitrifying bacteria were developed by batch incubation and immobilized with polyvinyl alcohol (PVA) on the surface of activated carbon fiber (ACF) to make a coated electrode. Then the coated electrode (cathode) and graphite electrode (anode) were transferred to the reactor to reduce nitrate. RESULTS: After acclimated to the mixtrophic and autotrophic denitrification stages, the denitrifying bacteria could use hydrogen as an electron donor to reduce nitrate. When the initial nitrate concentration was 30.2 mg NO3- -N / L, the denitrification efficiency was 57.3% at an applied electric current of 15 mA and a hydraulic retention time (HRT) of 12 hours. Correspondingly, the current density was 0.083 mA/cm2. The nitrate removal rate of the reactor was 34.4 g NO3- -N/m3 x d, and the surface area loading was 1.34 g NO3- -N / m2 x d. CONCLUSION: The coated electrode may keep high quantity of biomass, thus achieving a high denitrification rate. Denitrification efficiencies are related to HRT, current density, oxidation reduction potential (ORP), dissolved oxygen (DO), pH value, and temperature.

Adsorption↗
PubMed2005

Finite element formulation for a digital image correlation method.

A finite element formulation for a digital image correlation method is presented that will determine directly the complete, two-dimensional displacement field during the image correlation process on digital images. The entire interested image area is discretized into finite elements that are involved in the common image correlation process by use of our algorithms. This image correlation method with finite element formulation has an advantage over subset-based image correlation methods because it satisfies the requirements of displacement continuity and derivative continuity among elements on images. Numerical studies and a real experiment are used to verify the proposed formulation. Results have shown that the image correlation with the finite element formulation is computationally efficient, accurate, and robust.

Journal Article↗
PubMed2005

[Study on an epidemic caused by the vaccine-derived poliovirus circulation in Guizhou province, 2004].

OBJECTIVE: To study the circulating vaccine-derived poliovirus (cVDPVs) that occurred in Zhenfeng county, Guizhou province in 2004 and to discover wild-poliovirus, vaccine-derived poliovirus (VDPVs) and other vaccine-associated poliovirus which could cause clinical poliomyelitis. METHODS: Field epidemiological studies at the epidemic area and collecting acute flaccid paralysis (AFP) case and contact stool specimen for virus identification and nucleotide sequencing. Analysis on data related to annual reports on stool specimens surveillance which involved AFP case and contacts in the resent years in Zhenfeng county. RESULTS: Type-I VDPVs had been isolated from 2 AFP cases and 3 contact stool specimen in Wanlan village of Zhenfeng. After the first cVDPVs case was identified, there were 3 cases identified of having other vaccine-associated poliovirus of type-I or type-II in the 5 case of AFP that met the criteria of clinical poliomyelitis. The result of virological surveillance on polio showed that the EV isolation rate (55.1%) of Zhenfeng county was higher than the rate from the whole province of the same year (23.2%). The poliovirus (PV) isolation rate (36.8%) was obviously higher in 2004 than in the previous years. In the 16 PVs strains, the type-I accounted for 43.8% which was significantly higher than the average level (18.3%) from the whole province. CONCLUSIONS: Data indicated that the type-I VDPVs had been circulating (cVDPVs) in Zhenfeng county in Guizhou province. Clinical poliomyelitis was caused by non-VDPVs. The increased PV infection and the decreasing rate of vaccination in the general population were responsible for the epidemic of type-I cVDPVs at this time. Monitoring and evaluation on the rate of routine immunization program and prediction of the trend of epidemic should be strenthened.

Adolescent↗
PubMed2004

Structural evidence for direct hydride transfer from NADH to cytochrome P450nor.

Nitric oxide reductase cytochrome P450nor catalyzes an unusual reaction, direct electron transfer from NAD(P)H to bound heme. Here, we succeeded in determining the crystal structure of P450nor in a complex with an NADH analogue, nicotinic acid adenine dinucleotide, which provides conclusive evidence for the mechanism of the unprecedented electron transfer. Comparison of the structure with those of dinucleotide-free forms revealed a global conformational change accompanied by intriguing local movements caused by the binding of the pyridine nucleotide. Arg64 and Arg174 fix the pyrophosphate moiety upon the dinucleotide binding. Stereo-selective hydride transfer from NADH to NO-bound heme was suggested from the structure, the nicotinic acid ring being fixed near the heme by the conserved Thr residue in the I-helix and the upward-shifted propionate side-chain of the heme. A proton channel near the NADH channel is formed upon the dinucleotide binding, which should direct continuous transfer of the hydride and proton. A salt-bridge network (Glu71-Arg64-Asp88) was shown to be crucial for a high catalytic turnover.

Crystallography, X-Ray↗
PubMed2004

D88A mutant of cytochrome P450nor provides kinetic evidence for direct complex formation with electron donor NADH.

The haem-distal pocket of nitric oxide reductase cytochrome P450 contains many Arg and Lys residues that are clustered to form a putative access channel for NADH. Asp88 is the sole negatively charged amino acid in this positive charge cluster, and thus it would be interesting to know its functional role. Here we found the intriguing phenomenon that mutation at this site of P450nor (D88A or D88V) considerably decreased the overall nitric oxide reductase activity without blocking the reducing half reaction in which the ferric enzyme-NO complex is reduced with NADH to yield a specific intermediate (I). The results indicate that the catalytic turnover subsequent to the I formation was blocked by such mutation. This property of the mutants made it possible to perform kinetic analysis of the reduction step, which is impossible with the wild-type P450nor. These results are the first kinetic evidence for direct complex formation between P450nor and an electron donor (NADH or NADPH). The kinetic analysis also showed that the inhibition by chloride ions (Cl(-)) is competitive with respect to NAD(P)H, which highlights the importance of the binding site for Cl(-) (the anion hole) in the interaction with NAD(P)H. We also characterized another mutant (D393A) of P450nor. The results demonstrated that both Asp residues play important roles in the interaction with NADH, whereas the role of Asp88 is unique in that it must be essential for the release of NAD(+) rather than binding to NADH.

Animals↗
PubMed2004

Nitrous oxide-forming codenitrification catalyzed by cytochrome P450nor.

Intact cells of the denitrifying fungus Fusarium oxysporum were previously shown to catalyze codenitrification to form a hybrid nitrous oxide (N2O) species from nitrite and other nitrogen compounds such as azide and ammonia. Here we show that cytochrome P450nor can catalyze the codenitrification reaction to form N2O from nitric oxide (NO) but not nitrite, and azide or ammonia. The results show that the direct substrate of the codenitrification by intact cells should not be nitrite but NO, which is formed from nitrite by the reaction of a dissimilatory nitrite reductase.

Anaerobiosis↗
PubMed2003

Overexpression of WISP-1 down-regulated motility and invasion of lung cancer cells through inhibition of Rac activation.

Wnt-induced-secreted-protein-1 (WISP-1) is a cysteine-rich, secreted factor belonging to the CCN family. These proteins have been implicated in the inhibition of metastasis; however, the mechanisms involved have not been described. We demonstrated that overexpression of WISP-1 in H460 lung cancer cells inhibited lung metastasis and in vitro cell invasion and motility. We investigated the possibility that WISP-1 may regulate activation of Rac, a small GTPase important for cytoskeletal reorganizations during motility. In an indirect assay, WISP-1-expressing cells exhibited marked reduction in Rac activation compared with control cells. Blocking antibodies to alpha(v)beta(5) and alpha(1) integrins restored Rac activation in WISP-1 cells, suggesting that the inhibitory effect of WISP-1 on Rac lies downstream of integrins. Constitutively activated Rac mutant (RacG12V) was transfected into WISP-1 cells to restore Rac activation and these WISP-1/RacG12V transfectants were used for further studies. We performed microarray and real-time PCR analyses to identify genes involved in invasion that may be differentially regulated by WISP-1. Here, we showed decreased expression of metalloproteinase-1 (MMP-1) in WISP-1 cells compared with controls but increased expression in WISP-1/RacG12V cells. In an invasion assay across collagen I, an MMP-1 target matrix, WISP-1 cells were significantly less invasive compared with controls, whereas WISP-1/RacG12V cells showed elevated invasion levels. This work illustrates a negatively regulated pathway by WISP-1 involving integrins and Rac in the down-regulation of invasion.

CCN Intercellular Signaling Proteins↗
PubMed2002

WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase.

WISP-1 (Wnt-1-induced secreted protein) was identified as an oncogene regulated by the Wnt-1-beta-catenin pathway. WISP-1 belongs to the CCN family of growth factors, which are cysteine-rich, heparin-binding, secreted proteins associated with the extracellular matrix, and can interact with cellular integrins. Expression of WISP-1 in some cells results in transformation and tumorigenesis. Here it is shown that WISP-1 can activate the antiapoptotic Akt/PKB signaling pathway. It also is demonstrated that WISP-1 can prevent cells from undergoing apoptosis following DNA damage through inhibition of the mitochondrial release of cytochrome c and up-regulation of antiapoptotic Bcl-X(L). Furthermore, the results show that WISP-1 protects cells from p53-dependent cell death, but not Fas-ligand activated cell death, suggesting that there may be cross talk between the tumor suppressor protein p53 and WISP-1 signaling pathways. WISP-1 acts to block cell death at a late stage in the p53-mediated apoptosis pathway.

Animals↗
PubMed2002

[The studies and progress of MEMS-based micro surgical tools].

The MEMS-based micro surgical tools are a kind of new devices applied in the minimally-invasive surgery. This paper introduces their application background and basic technology first, and then lays emphasis on the typical research accomplishments in the world. Finally, the research activities in China and some of the difficulties about the work are discussed.

Biosensing Techniques↗
PubMed2002

[Experimental study on the potential carcinogenicity of cooking oil fume condensate].

The potential carcinogenicity of cooking oil fume condensate (COFC) to human was studied. Human embryo lung diploid fibroblast cell strain KMB-17 cell was applied to establish a human diploid cell transformation system in vitro. Different concentrations of COFC were added into the media and co-incubated with cells. The malignant degree of transformation was assessed by the biological characteristics of the cells. The concentrations of COFC within the dose range of the experiment could induce the malignant transformation of KMB-17 cell, and with a obvious dose-response relationship (r = 0.9811). Transformed cells have exhibited many characteristics associating with malignant transformation, such as loss of density and contact-dependent inhibition, growth at low serum concentration, agglutination by low concentration of Con A, alteration of karyotype from diploid to aneuploid, and lose of anchorage dependence. It suggested that the malignant transformation of human embryo lung diploid fibroblast cell strain KMB-17 cell could be induced by COFC, which might have potential carcinogenicity to human.

Air Pollutants↗