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This may occur partly because an increased HA-rich matrix may support invasion by providing cancer cells with a suitable microenvironment (Knudson et al, 1989), stimulate cell motility via interactions of HA with cell-surface receptors (Yang et al, 1993), or form a barrier for cancer cells against host immunocompetent cells (McBride and Bard, 1979).
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TNXB mediates interactions between cells and the extracellular matrix and may support the growth of epithelial tumors [ 36].
Because CXCR4 enhances cancer invasiveness by matrix metalloprotease-13 [ 25], which is important for invasion of cancer cells by degrading extracellular matrix, this data may support our results of enhanced-invasiveness via NO-CXCR4 signaling.
In contrast, N2 neutrophils may support tumor growth by producing pro-angiogenic factors and matrix-degrading enzymes, suppress anti-tumor immune responses and facilitate metastasis [ 21, 26- 28].
Therefore, analogous to the role of chondroitin-proteoglycans in the developing vulva, CEJ-1/B0280.5 may support actomyosin-mediated cytokinesis of polar bodies by generating a hydrated matrix.
The findings presented may support the design of new therapeutic strategies to prevent or slow down the Fe2+-catalyzed glycosylation of collagen and other matrix proteins.
This may support the otolith asymmetry hypothesis.
This may support the theory.
As thymic architecture plays a crucial role in naïve T cell development, a tissue specific scaffold that provides essential supporting matrix may assist in stem cell-based thymus regeneration to recreate complex organoids.
Our results support the hypothesis that high density of a matrix may result in high apoptosis rates or low proliferation of myoblasts [ 32].
The supports, described by a receptance matrix, may have arbitrary degrees of freedom, either translational or rotational.
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