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The glycosylation levels of proteins in cancer cells are closely related to cancer invasion and migration. CD44 is a transmembrane glycoprotein that is significantly overexpressed in a variety of tumor cells and has been proven to promote the migration and motility of cancer cells, but the effect of its N-glycosylation modification on CD44 protein function in tumors is less studied. Here, we investigated the effect of six N-glycan chains (N25/57/100/110/120/255) on CD44s localization, function and stability in hepatocarcinoma cells. When the six sites were mutated, we found that CD44s lost its membrane localization in Huh7 and MHCC-97H cells. On this basis, we identified three glycosylation sites on CD44s (N57, N100 and N110) that played key roles in intracellular localization. When N57, N100 and N110 were mutated together, CD44 localized to the cytoplasm, while another three-site mutant (N25/N120/N255) was still anchored to the membrane. In addition, the ability of CD44-N57Q/N100Q/N110Q to promote the metastasis and invasion of Huh7 and 97H cells was weakened compared with that of CD44-N25Q/N120Q/N255Q. Furthermore, CD44-N57Q/N100Q/N110Q accumulated abnormally in the ER, and a high level of the ER stress (ERS) marker BiP was detected at the same time compared with wild-type CD44. When the lysosome inhibitor CQ was added, the content of mutant protein that triggered ERS significantly increased, which indicated that the degradation mode of CD44-N57Q/N100Q/N110Q after ERS was mainly through the lysosomal pathway (ERLAD). The results revealed that the N-glycosylation sites N57, N100 and N110 mutated on CD44s affected its function and degraded it by lysosomes after triggering ERS. These findings provide data for new studies on ER-related degradation, further promote the study of the glycan chain function of CD44 and furnish new ideas for the treatment of liver cancer metastasis. • N57, N100 and N110 are crucial N-glycosylation sites for CD44 function of promoting metastasis in HCC. • The lack of glycan chains on N57, N100 and N110 leads to translocation from membrane to cytoplasm of CD44 in HCC cells. • CD44-N57Q/N100Q/N110Q is degraded through ERLAD after triggering ER stress. [ABSTRACT FROM AUTHOR]

We review possible architectures for 400 Gigabit Ethernet links based on advanced modulation formats for the first time. Their optical link power budget, digital complexity, and power dissipation are compared via simulations. The challenges of implementing the physical layer are discussed. [ABSTRACT FROM PUBLISHER]

N -glycosylation has been revealed to be tightly associated with cancer metastasis. As a key transferase that catalyzes the formation of β1,4 N -acetylglucosamine (β1,4GlcNAc) branches on the mannose core of N -glycans, N -acetylglucosaminyltransferase IVa (GnT-IVa) has been reported to be involved in hepatocellular carcinoma (HCC) metastasis by forming N -glycans; however, the underlying mechanisms are largely unknown. In the current study, we found that GnT-IVa was upregulated in HCC tissues and positively correlated with worse outcomes in HCC patients. We found that GnT-IVa could promote tumor growth in mice; notably, this effect was attenuated after mutating the enzymatic site (D445A) of GnT-IVa, suggesting that GnT-IVa regulated HCC progression by forming β1,4GlcNAc branches. To mechanistically investigate the role of GnT-IVa in HCC, we conducted GSEA and GO functional analysis as well as in vitro experiments. The results showed that GnT-IVa could enhance HCC cell migration, invasion and adhesion ability and increase β1,4GlcNAc branch glycans on integrin β1 (ITGB1), a tumor-associated glycoprotein that is closely involved in cell motility by interacting with vimentin. Interruption of β1,4GlcNAc branch glycan modification on ITGB1 could suppress the interaction of ITGB1 with vimentin and inhibit cell motility. These results revealed that GnT-IVa could promote HCC cell motility by affecting the biological functions of ITGB1 through N -glycosylation. In summary, our results revealed that GnT-IVa is highly expressed in HCC and can form β1,4GlcNAc branches on ITGB1, which are essential for interactions with vimentin to promote HCC cell motility. These findings not only proposed a novel mechanism for GnT-IVa in HCC progression but also revealed the significance of N -glycosylation on ITGB1 during the process, which may provide a novel target for future HCC therapy. • GnT-IVa enhances cell motility and correlates with poor outcomes of HCC. • GnT-IVa increases β1,4GlcNAc branches on ITGB1 to promote cell motility of HCC. • β1,4GlcNAc branches on ITGB1 affect interactions with vimentin in HCC. [ABSTRACT FROM AUTHOR]

A large amount of valuable research on black silicon (b-Si) nanostructures has pushed its use further into application in recent years. However, the research results to be found are all related to plane substrates. For an investigation of b-Si structures on curved surfaces, they were fabricated on hemispherical silicon lenses using inductively coupled plasma reactive ion etching. It was possible to achieve different structure morphologies according to the selected etching parameters, analogous to their fabrication on Si wafers. Scanning electron microscopy inspections of the structure morphology were carried out to study the homogeneity across the lens surface as well as the orientation of the structures. Simulations of the bent electric field within the etching chamber and the resulting ion trajectories explain the underlying etching process that creates structures approximately perpendicular to the curved lens surface. Optical reflectance measurements confirm the findings on homogeneity and orientation. [ABSTRACT FROM AUTHOR]

In this paper, a new type of shallow-water seismic survey vessel is proposed to solve the problem that the traditional seismic survey vessels cannot satisfy the requirements of the shallow-water marine resources exploration. To reveal the influence of shallow water effect on resistance and flow field, this research is to obtain the resistance and shallow-water characteristics of this shallow-water seismic survey vessel through ship model experiments and numerical methods. Firstly, the ship model experiment predicted the resistance at different speeds in shallow water and obtained the benchmark data to validate numerical methods. Then, the CFD methods were used to calculate the resistance of the ship in deep and shallow water. The numerical results are in good agreement with the experimental results. Finally, this paper provided details of the distribution of wave, pressure and flow fields at different water depth conditions in order to explain the causes of increased resistance in shallow water, providing a reference for the shallow-water seismic survey vessel design. • A new type of shallow-water seismic survey vessel with a wide flat bulbous bow is proposed in this paper. • The results show that the ship is affected by the shallow water effect, which dramatically increases the residual resistance. [ABSTRACT FROM AUTHOR]