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Figure 8 | Molecular Cancer

Figure 8

From: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation

Figure 8

Hypothesis for the assembly of CD63/β1-integrins/Timp1 complex along melanoma genesis. In the absence of Timp1, almost no association between CD63 and β1-integrins occurs in melan-a melanocytes, which might contribute to their anoikis sensitivity. The presence of these molecules in pre-malignant 4C melanocytes and 4C11- and 4C11+ melanoma cells result in the formation of CD63/β1-integrins/Timp1 complex and acquisition of anoikis-resistant phenotype. The absence of physical interaction between Timp1 and β1-integrins might result in a less efficient survival transduction pathway, differently of what is seen in melanoma cell lines, in which this complex seems to be more tightly assembled.

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