Cellular processes hijacked by cancer cells

Cell growth is driven by mitogen and growth factors binding to receptors such as Tyrosine Kinase receptors to trigger intracellular downstream signalling cascade. Tumour has reduced growth factors requirement due to their overexpression of growth factors, aberrant growth factor receptors such as truncated growth factors.

Once the transformed cells have proliferated to certain extent, they secrete more proteases such as metalloproteases (MMP) to break down the basement membrane. Fibroblasts (a type of long thin cells) underneath the basement membrane also contribute to this process. In addition, cancer cells hijack cellular cytoskeleton, cell-cell adhesion molecules and receptors to become mobile. This leads to the loss of cellular polarity from epithelial (oblong shape) to mesenchymal (elongated, fibroblast-like shape) transition. Recently discovered cancer cell movement is three-dimensional (3D) migration from amoeba (rounded shape) to mesenchymal transition. This is due to the cytoskeleton (the cell internal skeleton) and GTPases being hijacked to make collective cancer cell migration in 3D possible.

Metastasis - Alberts, B. (Bruce Alberts) et al. Molecular Biology of the Cell, 4th ed., New York - Garland, 2002, p. 1325:

Cancer cells proliferate, then break through the basal lamina or basement membrane to migrate into the capillary to find other suitable tissue sites for invasion and proliferation

Apart from that, cancer cells also hijack autophagy process (auto-: self + phagy: eating: so cell eating their own internal organelles or debris) to help cancer cells to stay dormant. Autophagy is the double-edge sword because it is either cancer protective or cancer promoting which depends on tumour types and stages. Autophagy promotes normal homeostasis so suppressed autophagy will promote tumour by disrupting cell normal health maintenance and leads to early tumorigenesis. In contrast, if autophagy is supressed at the early cancer stage, there will be no further progression, otherwise, later stage progression can occur.

Tumour mass cannot proliferate beyond 2mm in diameter without oxygen and nutrients, so by secreting Vascular Endothelial Growth Factor (VEGF) and other pro-angiogenic factors as false signal towards existing blood vessels, tumour encourages aberrant angiogenesis for rapid growth and metastasis. VEGF is one of the most potent angiogenic factors.

Note:

Angiogenesis: formation of new blood vessels from pre-existing vasculature.

Receptors: the protein on the cell membrane that recognize and bind to specific molecules such as growth factors or hormones to elicit a cascade of biological responses inside the cells.