Surface evolution and self assembly of epitaxial thin films: nonlinear and anisotropic effects

A strained epitaxial film can undergo surface instability and self assemble into discrete islands. The unique physical features of these islands make self-assembly an enabling technique for advanced device technology while control of the island size, shape, and alignment is critical. During the process of self-assembly, the stress field and the interface interaction have profound effects on the dynamics of surface evolution. In this dissertation, a continuum model is developed to study the nonlinear dynamics of surface pattern evolution and self assembly in epitaxial thin films. Within the framework of non-equilibrium thermodynamics, a nonlinear evolution equation is developed, and a spectral method is implemented for numerical simulations. The effects of stress and wetting are examined. It is found that, without wetting, the nonlinear stress field induces a “blow-up” instability. With wetting, the thin film self assembles into an array of discrete islands lying on a thin wetting layer. The dynamics of island formation and coarsening over a long time and a large area is well captured by the interplay of the nonlinear stress field and the wetting effect in the present model. For single-crystal epitaxy, the anisotropic material properties in the bulk and surface play important roles in the process of self assembly and pattern formation. In particular, this study investigates the effects of anisotropic mismatch stress and generally anisotropic elasticity. First, under an anisotropic mismatch stress, a bifurcation of surface pattern is predicted. The effect of anisotropic elasticity on pattern evolution is then investigated for two specific systems, one for SiGe films on Si substrates with different surface orientations, and the other for hexagonal silicides on Si substrates. It is shown that the consideration of elastic anisotropy reveals a much richer dynamics of surface pattern evolution as opposed to isotropic models. Based on the theoretical and numerical results from the present study, experimental approaches may be developed to control the size and organization of self assembled surface patterns in epitaxial systems.Engineering MechanicsAerospace Engineering and Engineering Mechanic

STAT3 potentiates RNA polymerase I-directed transcription and tumor growth by activating RPA34 expression

Background: Deregulation of either RNA polymerase I (Pol I)-directed transcription or expression of signal transducer and activator of transcription 3 (STAT3) correlates closely with tumorigenesis. However, the connection between STAT3 and Pol I-directed transcription hasn’t been investigated. Methods: The role of STAT3 in Pol I-directed transcription was determined using combined techniques. The regulation of tumor cell growth mediated by STAT3 and Pol I products was analyzed in vitro and in vivo. RNAseq, ChIP assays and rescue assays were used to uncover the mechanism of Pol I transcription mediated by STAT3. Results: STAT3 expression positively correlates with Pol I product levels and cancer cell growth. The inhibition of STAT3 or Pol I products suppresses cell growth. Mechanistically, STAT3 activates Pol I-directed transcription by enhancing the recruitment of the Pol I transcription machinery to the rDNA promoter. STAT3 directly activates Rpa34 gene transcription by binding to the RPA34 promoter, which enhances the occupancies of the Pol II transcription machinery factors at this promoter. Cancer patients with RPA34 high expression lead to poor survival probability and short survival time. Conclusion: STAT3 potentiates Pol I-dependent transcription and tumor cell growth by activating RPA34 in vitro and in vivo

Galectin-3 Is a Natural Binding Ligand of MCAM (CD146, MUC18) in Melanoma Cells and Their Interaction Promotes Melanoma Progression

Melanoma cell adhesion molecule (MCAM, CD146, MUC18) is a heavily glycosylated transmembrane protein and a marker of melanoma metastasis. It is expressed in advanced primary melanoma and metastasis but rarely in benign naevi or normal melanocytes. More and more evidence has shown that activation of the MCAM on cell surface plays a vital role in melanoma progression and metastasis. However, the natural MCAM binding ligand that initiates MCAM activation in melanoma so far remains elusive. This study revealed that galectin-3, a galactoside-binding protein that is commonly overexpressed in many cancers including melanoma, is naturally associated with MCAM on the surface of both skin and uveal melanoma cells. Binding of galectin-3 to MCAM, via O-linked glycans on the MCAM, induces MCAM dimerization and clustering on cell surface and subsequent activation of downstream AKT signalling. This leads to the increases of a number of important steps in melanoma progression of cell proliferation, adhesion, migration, and invasion. Thus, galectin-3 is a natural binding ligand of MCAM in melanoma, and their interaction activates MCAM and promotes MCAM-mediated melanoma progression. Targeting the galectin-3–MCAM interaction may potentially be a useful therapeutic strategy for melanoma treatment.</jats:p