Thus, there are several potential mechanisms of radiosensitisation by inhibitors of the EGFR family; they may include favourable cell cycle reorganisation and/or abrogation or attenuation of signals required for survival during cell cycle arrest.
Other genes with potential roles in cell wall reorganisation were down-regulated, such as an endoxyloglucan transferase (contig9845), which has a role in primary cell wall restructuring, as well as an alpha/beta hydrolase (contig12015) and a beta-expansin (contig9652) (Additional file 2).
In DENV-infected cells, vimentin reorganisation was seen where a cage of vimentin is formed, and it has been shown that vimentin is involved in the assembly of DENV 2 particles [ 9, 16].
Primary keratinocytes isolated from young hpm mice adhered well to ECM substrates but failed to spread, to proliferate and to survive in vitro, suggesting that the reduced β1 integrin levels are sufficient to promote adhesion but insufficient to appropriately activate signalling pathway(s) required for F-actin reorganisation, cell spreading and proliferation.
Such movement, deletion or introduction of genes or operons can create a problem for the cell, as the reorganisation of the genome may result in disruption of transcriptional circuitry controlling the expression levels of such genes.
However, EMT is a time-consuming cellular process, which consists of multiple biochemical events, such as activation of transcription factors, expression of specific cell-surface proteins, reorganisation and expression of cytoskeletal proteins, and changes in the expression of specific microRNAs (Kalluri and Weinberg, 2009).
Activation of PAK1 results in actin phosphorylation in breast cancer cells, leading to a reorganisation of the cytoskeleton that favours cell migration and invasiveness (Adam et al, 1998).
The PI3K-Akt signalling pathway is potentially implicated in a number of different functions, such as glucose metabolism, protein synthesis, receptor insertion, cytoskeletal reorganisation and cell proliferation, however, it is most commonly associated with cell survival by inhibiting the activation of proapoptotic proteins and transcription factors [21] [22].
To escape a dormant state, tumor cells must engage with the ECM via integrin receptor(s), inducing signalling that leads to cytoskeletal reorganisation and cell proliferation [ 60].
