In addition to the role of miR-200c and miR-141 in the phenotypic conversion of normal cells, dysregulation of normal patterns of miR-200c expression occurs in multiple types of cancer cells and is linked to tumor progression [2], [6], [12], [13], [14], [15].
Strikingly, many of these low frequency driver events occur in multiple tumor types, highlighting their potential clinical significance.
In conclusion, our observations indicate that aberrant multi-lineage transdifferentiation or lineage infidelity occurs frequently in multiple types of human cancer and may be a wide spread phenomenon.
The sequential types tend to recur and occur in multiple sites.
PDZ domains often occur in multiple copies within proteins, as well as in various combinations with other types of protein interaction modules and/or functional domains.
Dysregulation of miR-200c and miR-141 occurs in multiple cancer types [5], [11], [20], [21], [23], [24], [25], [26], and this dysregulation involves a compromise of the epigenetic state of the CpG island associated with miR-200c and miR141.
Expression of oestrogen receptor beta was exclusively nuclear and occurred in multiple cell types.
Within the neuronal population, DISC1 expression occurs in multiple cell types, including both glutamatergic and GABAergic cells.
Cytoplasmic polyadenylation facilitates PABP recruitment and occurs in multiple cell types across metazoans (e.g. oocytes, male germ cells, early embryos and neurons [ 13]).
These results indicate that injury-triggered EFA-6 relocalization occurs in multiple neuron types, irrespective of the site of injury and independent of the Sec7 or PH domains.
