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The topographical pattern of cell anchorage regulates the assembly of actin fibers (Fig. 2), mitochondrial activity (Fig. 5), and even cell viability in response to the surface area of cell adhesion and substrate rigidity (Fig. 3).
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When attached cells lose their anchorage, a form of cell death known as anoikis is induced.
In normal cells, FAK functions as an important regulator of cell motility, proliferation and anchorage-dependent cell survival [11], [12].
Similarly, BAP1-deficient uveal melanoma cells were less capable than control cells of anchorage independent growth in soft agar assays.
Indeed, cell transformation is expressed by the alteration of cell morphology, a disorganized pattern of colony growth and the acquisition of anchorage-independent growth which is predictive of their ability to induce tumors when injected into syngenic animals [ 33].
The in vitro colony-forming ability of cells growing under anchorage-independent conditions was further investigated.
The proliferation ability of one single cell in anchorage-dependent and anchorage-independent conditions was examined by colony formation assay in plates and soft agar, respectively.
Anchorage-independent growth ability, one hallmark of cell neoplastic transformation, was tested by soft agar assay.
More often, cell culture is dependent on proper anchorage of cells to the growth surface.
Anchorage-independent growth of cancer cells is a hallmark of cell transformation.
Its overexpression may therefore promote anchorage-independent growth by modifying the expression pattern of transmembrane glycoproteins.
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