Are the abilities of losing adhesion molecules, gaining receptors for Extracellular Matrix (ECM) proteins, having enzymes to digest ECM, and inducing angiogenesis inherent in all cells, similar to cancer cells and cells in early embryos?

Cancer Cell Abilities and Their Relationship to Early Embryonic Cells

The abilities that cancer cells acquire during malignant transformation, including loss of adhesion molecules, gain of ECM protein receptors, production of ECM-degrading enzymes, and induction of angiogenesis, are indeed inherent capabilities that exist in early embryonic cells but are normally tightly regulated in adult tissues. 1

Cellular Adhesion Properties

• During epithelial-mesenchymal transition (EMT), both cancer cells and embryonic cells show decreased expression of cell-cell adhesion molecules, particularly adherens junctions and desmosomes, which occurs through transcriptional repression by EMT transcription factors 1
• The cytoplasmic relocalization of adhesion proteins like E-cadherin via post-translational modifications is an early feature of both cancer progression and normal embryonic development 1
• Loss of apical-basal polarity is often the first event observed during EMT in both cancer and embryonic contexts, leading to destabilization of adhesion complexes 1

ECM Interaction Capabilities

• Both cancer cells and embryonic cells express receptors for extracellular matrix (ECM) proteins that facilitate migration through tissues 1
• The Boyden chamber assay demonstrates how cells must gain specific receptors for ECM proteins (like collagens and fibronectin) to enable haptotaxis - migration toward specific ECM components 1
• These ECM receptors, particularly integrins, are expressed during normal embryonic development but are typically suppressed in most adult tissues except during wound healing 2

ECM-Degrading Enzymes

• Both cancer cells and embryonic cells secrete matrix metalloproteinases (MMPs) that degrade the basement membrane and interstitial stroma to facilitate invasion 1, 3
• In cancer, these enzymes are inappropriately activated, while in embryonic development, they are precisely controlled to enable proper tissue formation and remodeling 3
• The degradation of ECM by these enzymes releases previously bound heparin-binding cytokines and growth factors that further promote cell migration and proliferation 4

Angiogenesis Induction

• Angiogenesis virtually never occurs physiologically in adult tissues except in the ovary, endometrium, and placenta, but is essential during embryonic development 4
• Cancer cells reactivate angiogenic pathways that are normally active during embryonic development but dormant in most adult tissues 1
• Both cancer cells and embryonic tissues can induce angiogenesis through secretion of factors like VEGF, which stimulates endothelial cell migration, proliferation, and tube formation 1

Regulatory Differences Between Cancer and Embryonic Cells

• While the capabilities are similar, the key difference lies in regulation - embryonic cells have precise temporal and spatial control of these processes, while cancer cells show dysregulated activation 1
• In embryonic development, these processes are tightly controlled by developmental signals and are self-limiting, whereas in cancer they become constitutively activated 5
• The tumor microenvironment shows altered ECM composition and density compared to embryonic tissues, with cancer-associated ECM being more rigid and disorganized 1

Molecular Mechanisms

• Both cancer and embryonic cells utilize similar signaling pathways to activate these capabilities, including EMT transcription factors like Snail, Slug, and Twist 1
• The switch from epithelial to mesenchymal phenotype involves changes in intermediate filaments from cytokeratin to vimentin in both contexts 1
• Matrix metalloproteinases (MMPs) play dual roles in both settings - they not only degrade ECM but also release and activate growth factors embedded within the matrix 6, 3

These cellular capabilities represent fundamental biological processes that are essential for embryonic development but are normally suppressed in adult tissues. Cancer cells reactivate these dormant embryonic programs through genetic and epigenetic alterations, effectively "hijacking" normal developmental processes to enable malignant progression 1, 4.