Статті в журналах: "HNEIL1"

1

Rieux, Charlotte, Stéphane Goffinont, Franck Coste, Zahira Tber, Julien Cros, Vincent Roy, Martine Guérin, et al. "Thiopurine Derivative-Induced Fpg/Nei DNA Glycosylase Inhibition: Structural, Dynamic and Functional Insights." International Journal of Molecular Sciences 21, no. 6 (March 17, 2020): 2058. http://dx.doi.org/10.3390/ijms21062058.

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DNA glycosylases are emerging as relevant pharmacological targets in inflammation, cancer and neurodegenerative diseases. Consequently, the search for inhibitors of these enzymes has become a very active research field. As a continuation of previous work that showed that 2-thioxanthine (2TX) is an irreversible inhibitor of zinc finger (ZnF)-containing Fpg/Nei DNA glycosylases, we designed and synthesized a mini-library of 2TX-derivatives (TXn) and evaluated their ability to inhibit Fpg/Nei enzymes. Among forty compounds, four TXn were better inhibitors than 2TX for Fpg. Unexpectedly, but very interestingly, two dithiolated derivatives more selectively and efficiently inhibit the zincless finger (ZnLF)-containing enzymes (human and mimivirus Neil1 DNA glycosylases hNeil1 and MvNei1, respectively). By combining chemistry, biochemistry, mass spectrometry, blind and flexible docking and X-ray structure analysis, we localized new TXn binding sites on Fpg/Nei enzymes. This endeavor allowed us to decipher at the atomic level the mode of action for the best TXn inhibitors on the ZnF-containing enzymes. We discovered an original inhibition mechanism for the ZnLF-containing Fpg/Nei DNA glycosylases by disulfide cyclic trimeric forms of dithiopurines. This work paves the way for the design and synthesis of a new structural class of inhibitors for selective pharmacological targeting of hNeil1 in cancer and neurodegenerative diseases.

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2

Jia, Lei, Vladimir Shafirovich, Nicholas E. Geacintov, and Suse Broyde. "Lesion Specificity in the Base Excision Repair Enzyme hNeil1: Modeling and Dynamics Studies†." Biochemistry 46, no. 18 (May 2007): 5305–14. http://dx.doi.org/10.1021/bi062269m.

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3

Krishnamurthy, Nirmala, Xiaobei Zhao, Cynthia J. Burrows, and Sheila S. David. "Superior Removal of Hydantoin Lesions Relative to Other Oxidized Bases by the Human DNA Glycosylase hNEIL1†." Biochemistry 47, no. 27 (July 2008): 7137–46. http://dx.doi.org/10.1021/bi800160s.

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4

Ocampo-Hafalla, Maria T., Alvin Altamirano, Ashis K. Basu, Michael K. Chan, Jose Eliseo A. Ocampo, Archie Cummings, Robert J. Boorstein, Richard P. Cunningham, and George W. Teebor. "Repair of thymine glycol by hNth1 and hNeil1 is modulated by base pairing and cis–trans epimerization." DNA Repair 5, no. 4 (April 2006): 444–54. http://dx.doi.org/10.1016/j.dnarep.2005.12.004.

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5

Zhang, Qiu-Mei, Shin-Ichiro Yonekura, Masashi Takao, Akira Yasui, Hiroshi Sugiyama, and Shuji Yonei. "DNA glycosylase activities for thymine residues oxidized in the methyl group are functions of the hNEIL1 and hNTH1 enzymes in human cells." DNA Repair 4, no. 1 (January 2005): 71–79. http://dx.doi.org/10.1016/j.dnarep.2004.08.002.

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6

Kakhkharova, Zarina I., Dmitry O. Zharkov, and Inga R. Grin. "A Low-Activity Polymorphic Variant of Human NEIL2 DNA Glycosylase." International Journal of Molecular Sciences 23, no. 4 (February 17, 2022): 2212. http://dx.doi.org/10.3390/ijms23042212.

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Human NEIL2 DNA glycosylase (hNEIL2) is a base excision repair protein that removes oxidative lesions from DNA. A distinctive feature of hNEIL2 is its preference for the lesions in bubbles and other non-canonical DNA structures. Although a number of associations of polymorphisms in the hNEIL2 gene were reported, there is little data on the functionality of the encoded protein variants, as follows: only hNEIL2 R103Q was described as unaffected, and R257L, as less proficient in supporting the repair in a reconstituted system. Here, we report the biochemical characterization of two hNEIL2 variants found as polymorphisms in the general population, R103W and P304T. Arg103 is located in a long disordered segment within the N-terminal domain of hNEIL2, while Pro304 occupies a position in the β-turn of the DNA-binding zinc finger motif. Similar to the wild-type protein, both of the variants could catalyze base excision and nick DNA by β-elimination but demonstrated a lower affinity for DNA. Steady-state kinetics indicates that the P304T variant has its catalytic efficiency (in terms of kcat/KM) reduced ~5-fold compared with the wild-type hNEIL2, whereas the R103W enzyme is much less affected. The P304T variant was also less proficient than the wild-type, or R103W hNEIL2, in the removal of damaged bases from single-stranded and bubble-containing DNA. Overall, hNEIL2 P304T could be worthy of a detailed epidemiological analysis as a possible cancer risk modifier.

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7

Kaplan. "Jón Hnefill Aðalsteinsson (1927-2010)." Journal of American Folklore 124, no. 494 (2011): 318. http://dx.doi.org/10.5406/jamerfolk.124.494.0318.

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8

Fleming, Aaron M., and Cynthia J. Burrows. "Formation and processing of DNA damage substrates for the hNEIL enzymes." Free Radical Biology and Medicine 107 (June 2017): 35–52. http://dx.doi.org/10.1016/j.freeradbiomed.2016.11.030.

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9

Schaller, F. "In memoriam Wilhelm K�hnelt 1905?1988." Biology and Fertility of Soils 9, no. 2 (April 1990): 91–92. http://dx.doi.org/10.1007/bf00335788.

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10

Sogawa, Chiharu, Kei Kumagai, Norio Sogawa, Katsuya Morita, Toshihiro Dohi, and Shigeo Kitayama. "C-terminal region regulates the functional expression of human noradrenaline transporter splice variants." Biochemical Journal 401, no. 1 (December 11, 2006): 185–95. http://dx.doi.org/10.1042/bj20060495.

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The NET [noradrenaline (norepinephrine) transporter], an Na+/Cl−-dependent neurotransmitter transporter, has several isoforms produced by alternative splicing in the C-terminal region, each differing in expression and function. We characterized the two major isoforms of human NET, hNET1, which has seven C-terminal amino acids encoded by exon 15, and hNET2, which has 18 amino acids encoded by exon 16, by site-directed mutagenesis in combination with NE (noradrenaline) uptake assays and cell surface biotinylation. Mutants lacking one third or more of the 24 amino acids encoded by exon 14 exhibited neither cell surface expression nor NE uptake activity, with the exception of the mutant lacking the last eight amino acids of hNET2, whose expression and uptake resembled that of the WT (wild-type). A triple alanine replacement of a candidate motif (ENE) in this region mimicked the influences of the truncation. Deletion of either the last three or another four amino acids of the C-terminus encoded by exon 15 in hNET1 reduced the cell surface expression and NE uptake, whereas deletion of all seven residues reduced the transport activity but did not affect the cell surface expression. Replacement of RRR, an endoplasmic reticulum retention motif, by alanine residues in the C-terminus of hNET2 resulted in a similar expression and function compared with the WT, while partly recovering the effects of the mutation of ENE. These findings suggest that in addition to the function of the C-terminus, the common proximal region encoded by exon 14 regulates the functional expression of splice variants, such as hNET1 and hNET2.

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11

Du, Caiwen, Bogui Wen, Derui Li, Yingcheng Lin, Yuwu Zheng, Xun Peng, Chaoqun Hong, et al. "Downregulation of Epstein-barr Virus-Encoded Latent Membrane Protein-1 by Arsenic Trioxide in Nasopharyngeal Carcinoma Cells." Tumori Journal 92, no. 2 (March 2006): 140–48. http://dx.doi.org/10.1177/030089160609200210.

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Aims and Background It was documented that nasopharyngeal carcinoma (NPC) is associated with Epstein-Barr virus (EBV) and that EBV-encoded latent membrane protein-1 expression (LMP1) plays an important role in the pathogenesis of NPC. In preclinical studies, arsenic trioxide (As2O3) has been identified as a promising anticancer agent for treatment of NPC. The purpose of this study is to investigate if this agent can inhibit the expression of LMP1 and therefore lead to growth inhibition of NPC cells in vitro. Methods LMP1-positive NPC cells, HNE1-LMP1, were treated with 3 umol/L of As2O3 for 96 hours. The LMP1 protein expression and mRNA level in HNE1-LMP1 cells were determined by western blot, confocal immunofluorescence staining and semiquantitative reverse transcriptase reaction (RT-PCR). Apoptosis was determined by light microscopy and the TUNEL method. Alterations in the cell cycle distribution were also investigated by flow cytometry. MTT assay and colony formation assay were used to detect the proliferation of the cells. The LMP1-negative parental cell lines HNE1 and HNE2 were used as control in an attempt to elucidate the role of LMP1 in the anticancer effect of As2O3 on NPC cells. Results The expression of LMP1 at the protein and mRNA level was reduced after exposure to 3 umol/L As2O3. This dose of As2O3 significantly induced apoptosis and growth retardation of HNE1-LMP1 cells. In addition, more HNE1-LMP1 cells were induced to G0/G1 and G2/M arrest. The same dose of As2O3 had a moderate effect on HNE1 and HNE2 cells. Conclusion Arsenic trioxide can inhibit LMP1 expression and dictate apoptosis and alterations of cell cycle distribution as well as growth retardation. LMP1-positive NPC cells are more sensitive to As2O3 treatment than LMP1-negative NPC cells.

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12

Bu, G., S. Rennke, and H. J. Geuze. "ERD2 proteins mediate ER retention of the HNEL signal of LRP's receptor-associated protein (RAP)." Journal of Cell Science 110, no. 1 (January 1, 1997): 65–73. http://dx.doi.org/10.1242/jcs.110.1.65.

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The 39 kDa receptor-associated protein (RAP) is a receptor antagonist that interacts with several members of the low density lipoprotein (LDL) receptor gene family. Upon binding to these receptors, RAP inhibits all ligand interactions with the receptors. Our recent studies have demonstrated that RAP is an endoplasmic reticulum (ER) resident protein and an intracellular chaperone for the LDL receptor-related protein (LRP). The HNEL sequence at the carboxyl terminus of RAP represents a novel ER retention signal that shares homology with the well-characterized KDEL signal. In the present study, using immunoelectron microscopy we demonstrate that cells stably transfected with human growth hormone (GH) tagged with either KDEL (GH + KDEL) or HNEL (GH + HNEL) signals exhibit ER and cis-Golgi localization typical of ER-retained proteins. Overexpression of not only GH + HNEL but also GH + KDEL cDNA in transfected cells results in saturation of ER retention receptors and secretion of endogenous RAP indicating that the two signals interact with the same ER retention receptor(s). The role of RAP in the maturation of LRP is further supported by the observation that functional LRP is reduced about 60% as a result of decreased intracellular RAP. Pulse-chase labeling and immunolocalization studies of ERD2.1 and ERD2.2 proteins in transfected cells demonstrate a long half-life and Golgi localization for both receptors. Finally, overexpression of either ERD2.1 or ERD2.2 proteins significantly increases the capacity of cells to retain both KDEL and HNEL-containing proteins. Taken together, our results thus demonstrate that ERD2 proteins are capable of retaining the novel ER retention signal associated with RAP.

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13

Gu, Jiajia, Li Yin, Jing Wu, Nan Zhang, Teng Huang, Kai Ding, Haixia Cao, Lin Xu, and Xia He. "Cetuximab and Cisplatin Show Different Combination Effect in Nasopharyngeal Carcinoma Cells Lines via Inactivation of EGFR/AKT Signaling Pathway." Biochemistry Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7016907.

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Nasopharyngeal carcinoma (NPC) is a common malignant cancer in South China. Cisplatin is a classical chemotherapeutic employed for NPC treatment. Despite the use of cisplatin-based concurrent chemoradiotherapy, distant failure still confuses clinicians and the outcome of metastatic NPC remains disappointing. Hence, a potent systemic therapy is needed for this cancer. Epidermal growth factor receptor (EGFR) represents a promising new therapeutic target in cancer. We predicted that combining the conventional cytotoxic drug cisplatin with the novel molecular-targeted agent cetuximab demonstrates a strong antitumor effect on NPC cells. In this study, we selected HNE1 and CNE2 cells, which have been proved to possess different EGFR expression levels, to validate our conjecture. The two-drug regimen showed a significant synergistic effect in HNE1 cells but an additive effect in CNE2 cells. Our results showed that cisplatin-induced apoptosis was significantly enhanced by cetuximab in the high EGFR-expressing HNE1 cells but not in CNE2 cells. Further molecular mechanism study indicated that the EGFR/AKT pathway may play an important role in cell apoptosis via the mitochondrial-mediated intrinsic pathway and lead to the different antitumor effects of this two-drug regimen between HNE1 and CNE2 cells. Thus, the regimen may be applied in personalized NPC treatments.

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14

Haider, Nezam, Ragavendra R. Baliga, Y. Chandrashekhar, and Jagat Narula. "Adrenergic Excess, hNET1 Down-Regulation, and Compromised mIBG Uptake in Heart Failure." JACC: Cardiovascular Imaging 3, no. 1 (January 2010): 71–75. http://dx.doi.org/10.1016/j.jcmg.2009.11.002.

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15

Yin, Wei, Jianfeng Xu, and Yanjiao Mao. "Synergistic effects of autophagy inhibitors combined with cisplatin against cisplatin-resistant nasopharyngeal cancer cells." Biochemistry and Cell Biology 99, no. 3 (June 2021): 322–29. http://dx.doi.org/10.1139/bcb-2020-0283.

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This study explored the synergistic effects of autophagy inhibitors combined with cisplatin against cisplatin-resistant nasopharyngeal cancer cells by treating HNE-1 and cisplatin (diamminedichloroplatinum; DDP)-resistant HNE1/DDP nasopharyngeal cancer cell lines with DDP, autophagy inhibitors, or a combination of autophagy inhibitors and DDP. Cell viability was determined via MTT (colorimetric) and colony-forming assays, and the rate of apoptosis was determined using propidium iodide (PI) and annexin V double-staining. The expressions of proteins were determined by Western blotting. For our in-vivo studies, a murine xenograft model was established to evaluate the anti-tumor effects of the combination of autophagy inhibitor and DDP. The results showed that treatment with DDP increased the expressions of ATP-binding cassette sub-family B member 1 (ABCB1), ATP Binding Cassette Subfamily C Member 1 (ABCC1), and P-glycoprotein 1 (P-gp) in the HNE1/DDP cell lines. Treatment with chloroquine decreased the expression levels of ABCB1, ABCC1, and P-gp, and increased the formation of LC3-II and the expression levels of p62 in the HNE1/DDP cells. Additionally, the combination of autophagy inhibitors and DDP produced a synergistic effect on DDP-induced cell death and apoptosis. Furthermore, the combination of the autophagy inhibitor and DDP showed significant anti-tumor effects in the xenograft mouse model. In summary, autophagy inhibitors show synergistic anti-tumor effects with DDP in vitro against DDP-resistant nasopharyngeal cancer cells and in vivo in our xenograft murine model.

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16

Giridhar, Prashanth, Supriya Mallick, Suman Bhasker, Sushmita Pathy, Bidhu Kalyan Mohanti, Ahitagni Biswas, and Atul Sharma. "Head and neck extra nodal NHL (HNENL) - Treatment Outcome and Pattern of failure - A Single Institution Experience." Asian Pacific Journal of Cancer Prevention 16, no. 15 (October 6, 2015): 6267–72. http://dx.doi.org/10.7314/apjcp.2015.16.15.6267.

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17

Stein, Karl, Moe Tun, Keith Musser, and Richard Rocheleau. "Evaluation of a 1 MW, 250 kW-hr Battery Energy Storage System for Grid Services for the Island of Hawaii." Energies 11, no. 12 (December 1, 2018): 3367. http://dx.doi.org/10.3390/en11123367.

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Battery energy storage systems (BESSs) are being deployed on electrical grids in significant numbers to provide fast-response services. These systems are normally procured by the end user, such as a utility grid owner or independent power producer. This paper introduces a novel research project in which a research institution has purchased a 1 MW BESS and turned ownership over to a utility company under an agreement that allowed the institution to perform experimentation and data collection on the grid for a multi-year period. This arrangement, along with protocols governing experimentation, has created a unique research opportunity to actively and systematically test the impact of a BESS on a live island grid. The 2012 installation and commissioning of the BESS was facilitated by a partnership between the Hawaii Natural Energy Institute (HNEI) and the utility owner, the Hawaiian Electric and Light Company (HELCO). After the test period ended, HELCO continued to allow data collection (including health testing). In 2018, after 8500 equivalent cycles, the BESS continues to operate within specifications. HNEI continues to provide HELCO with expertise to aid with diagnostics as needed. Details about the BESS design, installation, experimental protocols, initial results, and lessons learned are presented in this paper.

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18

Kaitai, Yao, Zhu Hecheng, Wang Fuxi, Li Guiyuan, Wen Dongsheng, and Li Yunping. "Establishment of a novel cell line (HNE1) derived from a nasopharyngeal carcinoma." Chinese Journal of Cancer Research 2, no. 2 (June 1990): 7–11. http://dx.doi.org/10.1007/bf02912241.

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19

ROBBI, Mariette, Emile VAN SCHAFTINGEN, and Henri BEAUFAY. "Cloning and sequencing of rat liver carboxylesterase ES-4 (microsomal palmitoyl-CoA hydrolase)." Biochemical Journal 313, no. 3 (February 1, 1996): 821–26. http://dx.doi.org/10.1042/bj3130821.

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A cDNA which encodes a carboxylesterase of 561 amino acid residues including a cleavable signal peptide is described. The enzyme expressed in COS cells migrates during PAGE (SDS-, and non-denaturing) as a single prominent band in the region of liver ES-4. It ends in the C-terminal cell-retention signal -HNEL, which, in COS cells overexpressing the enzyme, appears to be slightly less efficient than the signals -HTEL and -HVEL of ES-3 and ES-10 respectively. Glycosylation is not essential for intracellular retention, but leads to a higher activity. As do many carboxylesterases, the enzyme expressed in COS cells hydrolyses o-nitrophenyl acetate and α-naphthyl acetate. It also hydrolyses acetanilide, although less efficiently than ES-3, and, distinctively, palmitoyl-CoA. In addition to the four canonical Cys residues of the carboxylesterases, it contains a fifth, unpaired Cys336, which apparently is not essential for the catalytic properties. Indeed, treatment with iodoacetamide or substitution of Cys336 by Phe does not markedly alter the activity of the enzyme on the various substrates. The predicted structure of ES-4 is highly homologous to that of two other recently cloned esterases which also end in -HNEL [Yan, Yang, Brady and Parkinson (1994) J. Biol. Chem. 269, 29688–29696; Yan, Yang and Parkinson (1995) Arch. Biochem. Biophys. 317, 222–234]. Together, these isoenzymes probably account for the closely spaced bands observed in the region of ES-4 in non-denaturing PAGE.

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20

Krasavin, M. Y., M. A. Gureev, А. V. Garabadzhiu, A. Y. Pashkin, А. S. Zhukov, V. R. Khairutdinov, A. V. Samtsov, and V. I. Shvets. "Inhibition of neutrophil elastase and cathepsin G as a new approach to the treatment of psoriasis: from fundamental biology to development of new target-specific drugs." Доклады Академии наук 487, no. 4 (August 27, 2019): 455–59. http://dx.doi.org/10.31857/s0869-56524874455-459.

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Psoriasis therapy remains extremely relevant area of modern drug design, due to necessity of adverse reactions reduction, inherent for actual methods of therapy. It has been established that two of serine proteases are key agents in psoriasis development: neutrophil elastase 1 (HNE1) and cathepsin G (CatG). Collected molecular data for presented targets forms the basis of molecular modeling strategy for search and identification of new target-specific inhibitors. The result of work is a group of high-priority small-molecule compounds with double-targeted affinity with ability to suppress pro-psoriatic processes, induced by observed serine proteases in the initial stage of disease.

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21

Ward-Cook, Kory, and Peggy P. Simpson. "ASCP Board of Registry Statistics: January Through December 1999." Laboratory Medicine 31, no. 10 (October 2000): 555–56. http://dx.doi.org/10.1309/hnel-tlxl-0ph4-5rf9.

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22

Zhang, L., X. Jia, X. Liu, T. Sheng, R. Cao, Q. He, Z. Liu, et al. "Dataset of the plasma membrane proteome of nasopharyngeal carcinoma cell line HNE1 for uncovering protein function." Acta Biochimica et Biophysica Sinica 40, no. 1 (January 1, 2008): 55–70. http://dx.doi.org/10.1111/j.1745-7270.2008.00374.x.

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23

Peng, Cong, Hua Ying Liu, Ming Zhou, Li Ming Zhang, Xiao Ling Li, Shou Rong Shen та Gui Yuan Li. "BRD7 suppresses the growth of Nasopharyngeal Carcinoma cells (HNE1) through negatively regulating β-catenin and ERK pathways". Molecular and Cellular Biochemistry 303, № 1-2 (26 квітня 2007): 141–49. http://dx.doi.org/10.1007/s11010-007-9466-x.

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24

Yang, Shiming, Zhirao Dai, Weimin Li, Rongguan Wang, and Dongyan Huang. "Aberrant promoter methylation reduced the expression of protocadherin 17 in nasopharyngeal cancer." Biochemistry and Cell Biology 97, no. 4 (August 2019): 364–68. http://dx.doi.org/10.1139/bcb-2017-0343.

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This study aimed to explore the underlying mechanism of protocadherin 17 (PCDH17) downregulated in nasopharyngeal cancer (NPC). NPC tumor and adjacent tissue samples were collected from NPC patients who received therapy in the Chinese PLA General Hospital. Meanwhile, a normal epithelial cell lines NP96 and 6 NPC and cell lines C666-1, CEN1, CEN2, HNE1, HEN2, and HONE1 were prepared. Then, the expression level of PCDH17 and the methylation level of PCDH17 promoter in both tissues samples and cell lines were determined using the PCR method. Moreover, PCDH17 was overexpressed in CNE2 and HONE1 using Lipo2000. Following this, the proliferation and apoptosis of CNE2 and HONE1 were assessed using MTT and flow cytometry. The expression of PCDH17 was significantly downregulated in NPC tissues compared with the adjacent tissues as well as in the NPC cell lines compared with the normal NP96 cells. Overexpressed PCDH17 could significantly inhibit the proliferation of CNE2 and HONE1 cells but obviously promote the apoptosis of these two cell lines. Aberrant hypermethylation in the promoter might be the explanation of PCDH17 downregulated in PCDH17 and promoted the development of NPC.

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25

Post, R. M., G. S. Leverich, A. M. Speer, G. Xing, and S. R. B. Weiss. "Neural mechanisms of childhood-onset bipolar illness." Acta Neuropsychiatrica 12, no. 3 (September 2000): 139–43. http://dx.doi.org/10.1017/s0924270800035626.

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ABSTRACTSubstantial evidence exists for a cohort effect (earlier onset and increased prevalence) for both unipolar and bipolar affective disorder in every generation born since World War II. This effect could be related to inherited mechanisms (e.g., bi-Hneal pedigrees or genetic anticipation) or to environmental/experiential effects on gene expression (e.g., stressor effects on the induction of transcription and growth factors, enzymes, hormones and their receptors, and signal transduction molecules) as documented in preclinical models of neonatal maternal separation.This laboratory evidence is summarized and new clinical data on the impact of severe stressors on the unfolding course of bipolar illness are noted. The reported occurrence of childhood or adolescent physical or sexual abuse, compared to those who report their absence, is associated with: earlier bipolar illness onset; faster cycling (including ultradian) patterns; increased Axis I and II comorbidities; and increased time ill in a prospective year of follow-up. Selectively, physical abuse was associated with a reported pattern of increasingly severe mania and sexual abuse with increased numbers of serious suicide attempts.In a retrospective survey of parents of children with an approximate average age of 13 who were diagnosed with bipolar illness (compared to those with other diagnoses and those with no diagnosis), a cluster of symptoms related to irritability and dyscontrol differentiated the bipolar children earliest. These symptoms included: temper tantrums, irritability, inattention, hyperactivity, impulsivity, poor frustration tolerance, and increased aggression.Given the growing evidence that episodes of affective dysfunction can not only convey morbidity and mortality, but may also sensitize to further recurrence and thus change the course of illness, opportunities abound for early recognition and intervention in childhood onset bipolar illness. Such a successful endeavor would both allow a more normal psychobiological development and allow the possibility of preventing the unfolding of more full-blown bipolar illness altogether.

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26

ZHOU, H., G. LI, Y. YANG, X. LI, S. SHENG, W. ZHANG, and J. ZHAO. "Intracellular co-localization of SPLUNC1 protein with nanobacteria in nasopharyngeal carcinoma epithelia HNE1 cells depended on the bactericidal permeability increasing protein domain." Molecular Immunology 43, no. 11 (April 2006): 1864–71. http://dx.doi.org/10.1016/j.molimm.2005.10.021.

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27

Wang, Dingkun, Cheng Wu, Dongbo Liu, Linli Zhang, Guoxian Long, Guangyuan Hu, and Wei Sun. "Ginsenoside Rg3 Inhibits Migration and Invasion of Nasopharyngeal Carcinoma Cells and Suppresses Epithelial Mesenchymal Transition." BioMed Research International 2019 (February 24, 2019): 1–11. http://dx.doi.org/10.1155/2019/8407683.

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Nasopharyngeal carcinoma (NPC) is a highly invasive and metastatic head and neck cancer. Distant metastasis becomes the predominant mode of treatment failure in NPC patients. Ginsenoside Rg3 (Rg3), an active pharmaceutical component extracted from traditional Chinese medicine ginseng, shows antitumor effects in various cancers. In this study, we aimed to determine whether Rg3 inhibits the migration and invasion activity of NPC cells and to explore the possible mechanisms. Our results revealed that Rg3 hampers cell migration and invasion in both HNE1 and CNE2 cell lines. A reduced level of matrix metalloproteinase-2 (MMP-2) and MMP-9 was induced by Rg3 treatment. In addition, Rg3 significantly altered the expression of epithelial mesenchymal transition (EMT) markers with increased E-cadherin but decreased Vimentin and N-cadherin expression. Transforming growth factorβ- (TGF-β-) induced morphological transition and marker proteins change of EMT were reversed by Rg3. What is more, Rg3 suppressed the expression of EMT-related transcription factors, especially the Zinc Finger E-Box Binding Homeobox 1 (ZEB1). In summary, our data suggested that Rg3 could inhibit migration and invasion of NPC cells. This effect of Rg3 might be mediated through regulating MMP-2 and MMP-9 expressions and suppressing EMT. Thus, Rg3 may be a potentially effective agent for the treatment of NPC.

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28

Safady, Nágela Gomes, João R. S. Lopes, Carolina S. Francisco, and Helvécio Della Coletta-Filho. "Distribution and Genetic Diversity of Xylella fastidiosa subsp. pauca Associated with Olive Quick Syndrome Symptoms in Southeastern Brazil." Phytopathology® 109, no. 2 (February 2019): 257–64. http://dx.doi.org/10.1094/phyto-07-18-0273-fi.

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In Brazil, the host expansion of Xylella fastidiosa subsp. pauca was recently demonstrated with the report of diseased olive trees (Olea europaea), whose symptoms were associated with olive quick decline syndrome previously described in southern Italy. We employed both polymerase chain reaction-based techniques and culture medium isolation to investigate the geographic distribution of X. fastidiosa as well as the genetic signatures of 21 strains isolated from 11 olive orchards in both São Paulo and Minas Gerais States in Brazil. X. fastidiosa subsp. pauca was detected in 83% of the orchards examined in the region, and was positively diagnosed in 43.7% of all sampled plants with typical scorching symptoms. Of the 21 strains characterized with fast-evolving microsatellite (single sequence repeat [SSR]) markers, 20 different multilocus microsatellite genotypes were observed with the overall allelic diversity of HNei = 0.38. Principal component analysis using the SSR markers clustered all strains, except for three, in one cluster demonstrating a limited range of genetic diversity. Multilocus sequence typing analysis showed the prevalence of a sequence type (ST16) in 75% of the samples; three other novel STs (84, 85, and 86), were detected, all belonging to the X. fastidiosa subsp. pauca cluster. These results show that genetically diverse strains of X. fastidiosa subsp. pauca are widely present in olive orchards in southeastern Brazil, which is consistent with the long history of this bacterium in that region.

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Coletta-Filho, Helvécio D., Leonora S. Bittleston, and Rodrigo P. P. Almeida. "Spatial Genetic Structure of a Vector-Borne Generalist Pathogen." Applied and Environmental Microbiology 77, no. 8 (February 11, 2011): 2596–601. http://dx.doi.org/10.1128/aem.02172-10.

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ABSTRACTVector-borne generalist pathogens colonize several reservoir species and are usually dependent on polyphagous arthropods for dispersal; however, their spatial genetic structure is generally poorly understood. Using fast-evolving genetic markers (20 simple sequence repeat loci, resulting in a total of 119 alleles), we studied the genetic structure of the vector-borne plant-pathogenic bacteriumXylella fastidiosain Napa Valley, CA, where it causes Pierce's disease when it is transmitted to grapevines from reservoir plants in adjacent riparian vegetation. Eighty-three differentX. fastidiosamultilocus microsatellite genotypes were found in 93 isolates obtained from five vineyards, resulting in an index of clonal fraction closer to 0 and a Simpson's genotypic diversity index (D) closer to a maximum value of 1. Moderate values of Nei's gene diversity (HNei; averageHNei= 0.41) were observed for most of theX. fastidiosapopulations. The low Wright's index of genetic diversity among populations calculated by the FSTAT software (Wright'sFSTindex) among population pairs (0.0096 to 0.1080) indicated a weak or absent genetic structure among the five populations; a panmictic population was inferred by Bayesian analyses (with the STRUCTURE and BAPS programs). Furthermore, a Mantel test showed no significant genetic isolation by distance when both Nei (r= −0.3459,P= 0.268) and linearized θ (r= −0.3106,P= 0.269) indices were used. These results suggest that the riparian vegetation from which vectors acquire the pathogen prior to inoculation of grapevines supports a diverse population ofX. fastidiosa.

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Li, Jin-Yun, Wen-Xiao Huang, Jie Chen, Su-Ping Zhao, and Yao-Yun Tang. "Targeted Inhibitory Effect of Nasopharyngeal Carcinoma Cells by Hre2.Grp78 Chimeric Promoter Regulating Fusion Gene TK/VP3." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381987516. http://dx.doi.org/10.1177/1533033819875166.

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Objective: To construct plasmids with Hre2.Grp78 chimeric promoter regulating fusion gene TK/VP3 and elaborate the effects of overexpressed TK/VP3 on nasopharyngeal carcinoma cells. Methods: Four plasmids were constructed, including pcDNA3.1-CMV-TK/VP3, pcDNA3.1-Hre2.TK/VP3, pcDNA3.1-Grp78.TK/VP3, and pcDNA3.1-Hre2.Grp78.TK/VP3. The human nasopharyngeal carcinoma cell line HNE1 cells were transfected with the 4 plasmids, respectively. Cell viabilities were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and apoptosis was conducted using flow cytometry analysis. The expression of TK, VP3, Grp78, and hypoxia-inducible factor 1α and apoptosis-related proteins was determined by real-time quantitative polymerase chain reaction and Western blotting. Results: The recombinant plasmids that could steadily overexpress TK and VP3 were successfully constructed. Expression of TK and VP3 in cells transfected with pcDNA3.1-Hre2.TK/VP3 and pcDNA3.1-Grp78.TK/VP3 was significantly higher than pcDNA3.1-CMV-TK/VP3, and expression in cells transfected with pcDNA3.1-Hre2.Grp78.TK/VP3 was the highest. Under glucose deprivation or hypoxia condition, Grp78 or hypoxia-inducible factor 1α was overexpressed so that expression of TK and VP3 was significantly upregulated, which could further inhibit cell proliferation and enhance cell apoptosis. Conclusion: We successfully constructed 4 plasmids with Hre2.Grp78 chimeric promoter regulating fusion gene TK/VP3, which could significantly inhibit the proliferation as well as enhance the apoptosis of nasopharyngeal carcinoma cells under glucose deprivation or hypoxia condition.

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Xu, Sheng, and Wenxia He. "Effect of miR-200c on nasopharyngeal carcinoma and the probable molecular regulatory mechanism involved." Tropical Journal of Pharmaceutical Research 20, no. 1 (March 17, 2021): 41–46. http://dx.doi.org/10.4314/tjpr.v20i1.7.

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Purpose: To determine the effect of micro-ribonucleic acid-200c (miR-200c) on biological function of nasopharyngeal carcinoma, and the likely molecular regulatory mechanism involved.Methods: Thirty (30) nasopharyngeal carcinoma tissues and para-cancerous normal tissues were taken from patients undergoing surgery in Maternal and Child Health Hospital of Hubei Province, Wuhan from September 2018 to January 2020. The expression levels of miR-200c in the two types of tissues were determined. Cells of human nasopharyngeal carcinoma cell line HNE1 were cultured to about 70 % growth prior to transfection with blank plasmid, PINI and miR-200c analogs. After 48 h of culture, control group, PINI group, and miR-200c over-expression + PINI group were obtained. The expression levels of PINI and changes in centrosomes in each group were measured, and changes in cell migration in each group were determined using Transwell migration assay.Results: Compared with para-cancerous normal tissues, the expression level of miR-200c in nasopharyngeal carcinoma was significantly increased (p < 0.01). Compared with the control group, the PINI expression level and cell migration ability in miR-200c overexpression tissue were markedly decreased, while the percentage of extra centrosomes was markedly increased. Compared to miR-200c over-expression tissue, the PINI expression level and cell migration ability in the miR-200c overexpression + PINI group were markedly raised, while the percentage of extra-central somatic cells was significantly decreased (p < 0.05).Conclusion: MiR-200c may inhibit the migration of nasopharyngeal carcinoma cells by inhibiting the expression of PINI and inhibiting abnormal expansion of centrosomes. Keywords: MiR-200c, Nasopharyngeal carcinoma, Biological function, Molecular regulatory mechanism

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Wu, Hanwei, Yuchen Liu, Hongfang Duan, Xiaoqin Fan, Yujie Wang, Jian Song, Jinghong Han, Ming Yang, Lu Lu, and Guohui Nie. "Identification of differentially expressed circular RNAs in human nasopharyngeal carcinoma." Cancer Biomarkers 29, no. 4 (November 20, 2020): 483–92. http://dx.doi.org/10.3233/cbm-201731.

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BACKGROUND: Circular RNAs (circRNAs) are endogenous RNAs that have a covalent closed cycle configuration. circRNAs have been found to be differentially expressed in many human cancers. Therefore, circRNAs may be ideal biomarkers for the diagnosis and treatment of cancer. However, we know very little about the function of circRNAs in nasopharyngeal carcinoma (NPC). The purpose of this study was to evaluate the circRNA expression profiles in NPC. METHODS: We utilized high-throughput RNA sequencing (RNA-Seq) to evaluate the circRNA expression profile in NPC A total of 13,561 unique circRNA candidates were detected. Selection of aberrantly expressed circRNAs was carried out using a q-value of < 0.001 with a fold change of > 2.0 or < 0.5. We carried out Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses to identify the biological functions of differentially expressed circRNAs. Moreover, bioinformatics analyses were implemented to predict the effects between circRNAs and cancer-related microRNAs (miRNAs), and we used Cytoscape to build a cancer-related circRNA-miRNA target gene map. Finally, to verify dysregulated circRNAs, quantitative real-time PCR was utilized. RESULTS: In NPC tissues, we found that 73 circRNAs were downregulated and 59 were upregulated. The top 12 candidate circRNAs were selected from several vital NPC pathways such as the human papillomavirus and Epstein-Barr virus infection signaling pathways (hsa05165 and hsa05169, respectively), Hepatitis B (hsa05161), and the Ras signaling pathway (hsa04014). A network map of circRNA-miRNA interactions of 12 differentially expressed circRNAs was built. Hsa_circ_0007637 expression distinguished NPC tissues from paired healthy tissues and NPC cell lines (HNE1 6-10B, 5-8F, CNE-2, and so on) from a normal epithelial (NP460) cell line. CONCLUSIONS: In this study, we investigated the profiles of differentially expressed circRNAs in NPC, and our results show that hsa_circ_0007637 may be a biomarker for NPC and play a role in its development. This observation-based research identified dysregulated circRNAs in NPC, which may assist in the development of biomarkers for this disease. Further studies on the mechanisms and functions of these circRNAs may promote our understanding of NPC tumorigenesis.

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Liu, Menghao, Jun Zhang, Chenxu Zhu, Xiaoxue Zhang, Weide Xiao, Yongchang Yan, Lulu Liu, Hu Zeng, Yi Qin Gao, and Chengqi Yi. "DNA repair glycosylase hNEIL1 triages damaged bases via competing interaction modes." Nature Communications 12, no. 1 (July 5, 2021). http://dx.doi.org/10.1038/s41467-021-24431-y.

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AbstractDNA glycosylases must distinguish the sparse damaged sites from the vast expanse of normal DNA bases. However, our understanding of the nature of nucleobase interrogation is still limited. Here, we show that hNEIL1 (human endonuclease VIII-like 1) captures base lesions via two competing states of interaction: an activated state that commits catalysis and base excision repair, and a quarantine state that temporarily separates and protects the flipped base via auto-inhibition. The relative dominance of the two states depends on key residues of hNEIL1 and chemical properties (e.g. aromaticity and hydrophilicity) of flipped bases. Such a DNA repair mechanism allows hNEIL1 to recognize a broad spectrum of DNA damage while keeps potential gratuitous repair in check. We further reveal the molecular basis of hNEIL1 activity regulation mediated by post-transcriptional modifications and provide an example of how exquisite structural dynamics serves for orchestrated enzyme functions.

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Rocha, Susana, Rute Rebelo, Célia Amorim, Rui Moreira, Alice Santos-Silva, and Maria Conceição Branco Da Silva Montenegro. "MO752: Doping Polysulfone Dialysis Membranes with Human Neutrophil Elastase Inhibitors—A Proof-of-Concept Study." Nephrology Dialysis Transplantation 37, Supplement_3 (May 2022). http://dx.doi.org/10.1093/ndt/gfac079.031.

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Abstract BACKGROUND AND AIMS The recurrent contact of blood with the haemodialysis (HD) membrane during the treatment procedure, triggers neutrophil activation, leading to an increase of blood levels of neutrophil elastase that contributes to the chronic inflammatory response experienced by end-stage renal disease patients with a consequent increase of morbidity and mortality. Based on our group's experience in developing flat-sheet polysulfone (PSF) membranes by using the spin-coating and phase-inversion methods [1], and in the synthesis of human neutrophil elastase inhibitors (HNEIs), namely 4-oxo-β-lactam-based compounds [2], the successful doping of PSF membranes with HNEIs has been achieved [3]. These PSF-HNEI biomaterials have proven to be bioactive and biocompatible, and they included in house synthetized HNEIs alongside Sivelestat (SIV, a second generation HNEI) PSF membranes [3]. In this study, we took a step forward aiming to test the efficacy of such modified membranes when exposed to biological conditions (human plasma). METHOD SIV (Abcam) and an in house synthesized 4-oxo-β-lactam-based compound (D4L-2) [2], from our library, were used. The IC50 of both HNEIs in HEPES buffer was evaluated by performing an HNE activity assay [2]. PSF membranes were prepared as described elsewhere [1] and doped with each HNEI by adsorption [3]. In 3 independent assays, triplicates of PSF membrane circles (Ø = 0.6 cm) were incubated with HNEIs vehicle (2.5% DMSO) or with 10–2000 nM SIV or D4L-2 during 3 h at 25°C, for HNEIs adsorption. Afterwards, all PSF-HNEI membranes were incubated in diluted plasma (50% PBS, pH 7.4) or HEPES buffer for 3 h at 37°C. The bioactivity of PSF-HNEI membranes was assessed before and after incubation using the HNE activity assay [2]. The value obtained for PSF membranes incubated with HNEIs vehicle was used to normalize the results (0% HNE inhibition). RESULTS The IC50 of SIV and D4L-2 in solution were 32.7 and 18.1 nM, respectively. Before incubation with either plasma or HEPES buffer, the HNE inhibition capacity of both PSF-HNEI membranes increased in a concentration-dependent manner, reflecting the HNEIs solutions used during the adsorption process. The highest HNE inhibition ability was presented by PSF-D4L-2 membranes (91.7% ± 0.9% versus 35.3% ± 5.0%). After incubation, PSF-HNEIs membranes immersed in HEPES buffer showed a similar HNE inhibition (84.5% ± 2.2% and 34.0% ± 6.2% for D4L-2 and SIV, respectively). However, the modified membranes incubated in plasma showed a significant decrease in HNE inhibition (D4L-2: 23.7% ± 1.6% and SIV: 7.0% ± 2.1%). CONCLUSION D4L-2 showed the best performance (lower IC50 value and higher HNE inhibitory capacity of doped membranes), which is in accordance with following the assumption that the 4-oxo-β-lactam-based inhibitors are more stable molecules and present higher specificity for HNE. However, both PSF-HNEI biomaterials seem to have fulfiled the objective for which they were developed, since, after being incubated in plasma, they presented a significant decrease in the capacity to inhibit HNE, showing that the HNEIs immobilized in the membranes had captured/bound to the HNE present in the plasma sample.

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Heimerl, Maren, Irina Sieve, Melanie Ricke-Hoch, Sergej Erschow, Karin Battmer, Michaela Scherr, and Denise Hilfiker-Kleiner. "Neuraminidase-1 promotes heart failure after ischemia/reperfusion injury by affecting cardiomyocytes and invading monocytes/macrophages." Basic Research in Cardiology 115, no. 6 (September 25, 2020). http://dx.doi.org/10.1007/s00395-020-00821-z.

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Abstract Neuraminidase (NEU)1 forms a multienzyme complex with beta-galactosidase (β-GAL) and protective-protein/cathepsin (PPC) A, which cleaves sialic-acids from cell surface glycoconjugates. We investigated the role of NEU1 in the myocardium after ischemia/reperfusion (I/R). Three days after inducing I/R, left ventricles (LV) of male mice (3 months-old) displayed upregulated neuraminidase activity and increased NEU1, β-GAL and PPCA expression. Mice hypomorphic for neu1 (hNEU1) had less neuraminidase activity, fewer pro-inflammatory (Lin−CD11b+F4/80+Ly-6Chigh), and more anti-inflammatory macrophages (Lin−CD11b+F4/80+Ly-6Clow) 3 days after I/R, and less LV dysfunction 14 days after I/R. WT mice transplanted with hNEU1-bone marrow (BM) and hNEU1 mice with WT-BM showed significantly better LV function 14 days after I/R compared with WT mice with WT-BM. Mice with a cardiomyocyte-specific NEU1 overexpression displayed no difference in inflammation 3 days after I/R, but showed increased cardiomyocyte hypertrophy, reduced expression and mislocalization of Connexin-43 in gap junctions, and LV dysfunction despite a similar infarct scar size to WT mice 14 days after I/R. The upregulation of NEU1 after I/R contributes to heart failure by promoting inflammation in invading monocytes/macrophages, enhancing cardiomyocyte hypertrophy, and impairing gap junction function, suggesting that systemic NEU1 inhibition may reduce heart failure after I/R.

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"Synthesis and Structural Studies on some Dioxomolybdenum (VI) Complexes Bearing 1-(1-Hydroxynaphthalen-2-yl) Ethanone Moiety." Journal of Chemistry: Education Research and Practice 3, no. 1 (June 28, 2019). http://dx.doi.org/10.33140/jcerp.03.01.03.

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A number of new molybdenum complexes Cis-MoO2 (NE)2 .CH3 OH, Cis-MoO2 (HRSB)2 .nH2 O {R= H, 4-Br, 4-OCH3 , 4-CH3 and n= 0, 1, 2} Cis-MoO2 (HL)(acac).nH2 O {HL= HNEBH, HNEINH, HNENH, HNEPH, n=0, 1}, Cis-[MoO2 (L\)2 .nH2 O], {L\= HNE-2-ABH, HNE-4-ABH, n = 0, 2} and Cis-[Mo2 O5 (HNEAH)2 ] have been synthesized and characterization by magnetic, spectroscopic (FT-IR, 1H and 13C-NMR spectra) and electrochemical techniques. The complexes were made reaction of Cis-MoO2 (acac)2 with the ligands, (1-hydroxynaphthalen-2-yl)ethenone (HNE), (E)-2-(1-(phenylimino)ethyl)naphthalen1-ol (HASB), (E)-2-(1-(p-tolylimino)ethyl) naphthalen-1-ol (HTSB), E-2-(1-(4-methoxyphenylimino)ethyl)naphthalen-1-ol (HMSB) and (E)-2-(1-(4-bromophenylimino)ethyl)naphthalen-1-ol (HBrSB) monobasic bidentate (NO) or 2-anmino-N/- (1-(1-hydroxynaphthalene-2-yl)ethylidene)benzohydrazide (HNE2-ABH), 4-anmino-N/-(1-(1-hydroxynaphthalene-2-yl) ethylidene)benzohydrazide (HNE4-ABH), N/-(1-(1-hydroxynaphthalene-2-yl)ethylidene)benzohydrazide (HNEBH), N-(1-(1-hydroxynaphthalene-2-yl)ethylidene)acetohydrazide (HNEAH), N/-(1-(1-hydroxynaphthalene-2-yl)ethylidene) nicotinohydrazide (HNENH), N/-(1-(1-hydroxynaphthalene-2-yl)ethylidene)isonicotinohydrazide (HNEINH), N/-(1- (1-hydroxynaphthalene-2-yl)ethylidene)picolinohydrazide (HNEPH), they coordinate as dibasic tridentate (OON). Both the molecular and the spectroscopic studies showed that, the complexes are octahedrally coordinated. The redox properties, of the electrode couples and the stability of some complexes towards reduction were linked to the electron withdrawing or ability releasing of the substituent in the Schiff bases and the hydrazones. Results show that, changes in E1/2 for the complexes due to remote substituent effects could be related to changes in basicity of the carbonyl oxygen of the hydrazide moiety in the hydrazone ligand. The electron-donating substituents stabilized Mo(VI) complexes while electron-withdrawing groups favored lower oxidation state of Mo(V) and/ or Mo(IV) species. The nature of mechanism and kinetic parameters of the electroactive chelates are strongly dependent on the substituent. The EHOMO and ELUMO level, of hydrazone and some of Cis-molybdenum complexes, from both electrochemical and theoretical data also backdonation energy (ΔEback-donation), ionization potential (I), molecular dipole moment (μ), electronegativity (χ), softness (σ) electron affinity (A), global hardness (η), and electrophilicity index (ω) were calculated.

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"HNEI and Sierra Lobo demo PEMFCs for He recovery at NASA." Fuel Cells Bulletin 2014, no. 6 (June 2014): 11. http://dx.doi.org/10.1016/s1464-2859(14)70178-6.

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Kaneshiro, Jess M., Alexander Deangelis, Xi Song, Nicolas Gaillard, and Eric L. Miller. "I-III-VI2 (Copper Chalcopyrite-based) Thin Films for Photoelectrochemical Water-Splitting Tandem-Hybrid Photocathode." MRS Proceedings 1324 (2011). http://dx.doi.org/10.1557/opl.2011.964.

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ABSTRACTThis presentation will investigate various parameters regarding the use of I-III-VI2 Copper Chalcopyrite-based materials for use in tandem-hybrid photocathodes capable of splitting water into hydrogen and oxygen gases in an acidic electrolyte. Constituent parts (fabricated at HNEI) of a proposed monolithically integrated hybrid photovoltaic/photoelectrochemical (PV/PEC) device were characterized separately and combined theoretically using electronic and optical models to simulate tandem operation to first indicate feasibility of matching existing materials. Robust CGSe2 photocathodes were focused on for the PEC cells and CIGSe2 and CISe2 devices were evaluated for the PV cells. Simulation suggested the hybrid PV/PEC system could pass enough light to produce up to 15.87mA/cm2, validating the feasibility and warranting the fabrication of stacked PV/PEC devices.

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"Jón Hnefill Aðalsteinsson, A Piece of Horse Liver: Myth, Ritual and Folklore in Old Icelandic Sources. Trans. Terry Gunnell and Joan Turville-Petre. Reykjavík: Háskólaútgáfan, 1998. Paper. Pp. 188; tables." Speculum 75, no. 03 (July 2000): 749. http://dx.doi.org/10.1017/s0038713400197891.

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Jiang, Chang, Hongyan Li, Fei Liu, Linggai Shi, Jun Liu, and Yujie Li. "Hsa_circ_0000345 inhibits cell proliferation, migration and invasion of nasopharyngeal carcinoma cells via miR-513a-3p/PTEN axis." Journal of Physiological Sciences 72, no. 1 (May 12, 2022). http://dx.doi.org/10.1186/s12576-022-00834-4.

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Abstract Background Hsa_circ_0000345 has been reported to be down-regulated in nasopharyngeal carcinoma (NPC). Whether hsa_circ_0000345 can exert antitumor effect in NPC remains unclear. This study aimed to investigate the possible biological role of hsa_cic_0000345 in suppressing the progression of NPC. Methods Hsa_circ_0000345 expression was detected in normal nasopharynx epithelial cells (NP69) and NPC cell lines (SUNE1, HONE1, 6-10B and HNE1). The influence of hsa_circ_0000345 on cell proliferation, migration and invasion of NPC cells was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Quantitative real-time PCR and western blot were performed to examine gene and protein expression, respectively. Luciferase reporter assay was carried out to verify the relationship among hsa_circ_0000345, miR-513a-3p and phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Results Compared with NP69 cells, hsa_circ_0000345 was down-regulated in NPC cells. Moreover, hsa_circ_0000345 overexpression repressed cell proliferation, migration and invasion of SUNE1 cells, whereas hsa_circ_0000345 knockdown promoted cell proliferation, migration and invasion of 6-10B cells. Furthermore, hsa_circ_0000345 promoted PTEN expression by sponging miR-513a-3p. Both miR-513a-3p overexpression and PTEN knockdown promoted cell proliferation, migration and invasion of SUNE1 cells, which were effectively abolished by hsa_circ_0000345 up-regulation. Conclusion Hsa_circ_0000345 inhibits cell proliferation, migration and invasion of NPC cells via miR-513a-3p/PTEN axis, thereby suppressing the progression of NPC. Thus, this work suggests that hsa_circ_0000345 may be a potential biomarker for diagnosis and treatment of NPC.

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Zhou, Zun-Yan, Ji-Yuan Yang, Cheng-Ze Shao, Fei Luo, and Wei Du. "Positive regulation of ataxia-telangiectasia-mutated protein (ATM) by E2F transcription Factor 1 (E2F-1) in cisplatin-resistant nasopharyngeal carcinoma cells." World Journal of Surgical Oncology 20, no. 1 (March 18, 2022). http://dx.doi.org/10.1186/s12957-022-02546-w.

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Abstract Objective To explore the mechanism of E2F transcription Factor 1 (E2F-1)-mediated ataxia-telangiectasia-mutated protein (ATM) in cisplatin (DDP)-resistant nasopharyngeal carcinoma (NPC). Methods E2F-1 and ATM expression was assessed in DDP-resistant NPC cell lines (CNE2/DDP and HNE1/DDP) and parental cells. Then, DDP-resistant NPC cells were transfected with control shRNA (short hairpin RNA) or E2F-1 shRNAs with or without ATM lentiviral activation particles. The half maximal inhibitory concentration (IC50) was evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, and the cell cycle and cell proliferation were measured by flow cytometry and EdU staining, respectively. In addition, the expression of genes and proteins was quantified by quantitative reverse-transcription polymerase chain reaction (qRT–PCR) and western blotting, respectively. Results Both E2F-1 and ATM expression in DDP-resistant NPC cells was much higher than that in parental cells. E2F-1 shRNA reduced ATM expression in DDP-resistant NPC cells, but ATM overexpression had no significant effect on E2F-1. ATM overexpression enhanced DDP resistance in DDP-resistant NPC cells with increased IC50 values, which was reversed by E2F-1 inhibition. Meanwhile, ATM overexpression resulted in upregulation of ABCA2 and ABCA5 in DDP-resistant NPC cells, induced elevations in the transition of the cells into S-phase, and increased cell proliferation with enhanced expression of cyclin E1, CDK2, and Ki67, which was reversed by E2F-1 shRNAs. Conclusion Downregulation of E2F-1, possibly by regulating ATM, could block the cell cycle in the G1 phase and reduce the proliferation of CNE2/DDP cells, thereby reversing the resistance of human NPC cells to DDP.

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