[Cancer cell plasticity and metastatic dissemination].
Metastatic dissemination consists of a sequence of events resulting in the invasion by cancer cells of tissues located away from the primary tumour. This process is highly inefficient, since each event represents an obstacle that only a limited number of cells can overcome. However, two biological phenomena intrinsically linked with tumour development facilitate the dissemination of cancer cells throughout the body and promote the formation of metastases, namely the genetic diversity of cancer cells within a given tumour, which arises from their genetic instability and from successive clonal expansions, and cellular plasticity conveyed to the cells by micro-environmental signals. Genetic diversity increases the probability of selecting cells that are intrinsically resistant to biological and physical constraints encountered during metastatic dissemination, whereas cellular plasticity provides cells with the capacity to adapt to stressful conditions and to changes in the microenvironment. The epithelial-mesenchymal transition, an embryonic trans-differentiation process frequently reactivated during tumour development, plays an important role in that context by endowing tumor cells with a unique capacity of motility, survival and adaptability to the novel environments and stresses encountered during the invasion-metastasis cascade.
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Caroline
C
Moyret-Lalle
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Roxane
R
Pommier
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Charlotte
C
Bouard
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Ebticem
E
Nouri
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Geoffrey
G
Richard
Université de Lyon, Université Claude Bernard Lyon 1, Inserm 1052, CNRS 5286, Centre Léon Bérard, Centre de recherche en cancérologie de Lyon, 28, rue Laënnec, 69008 Lyon, France.
Alain
A
Puisieux
D000818:Animals; D000066670:Cell Plasticity / Q000502:physiology*; D018450:Disease Progression; D058750:Epithelial-Mesenchymal Transition; D006801:Humans; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000473:pathology*; D059016:Tumor Microenvironment / Q000502:physiology