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Loss of caspase-8 in tumor cells: mechanism to overcome integrin-mediated death?

Successful metastasis is determined by the ability of tumor cells to invade surrounding tissue, survive in the circulation, extravasate, arrest, and proliferate within the secondary organ. During this process, mutations in oncogenes and tumor suppressor genes lead to genetic instability, which bestow tumor cells with a selective growth advantage and aid the acquisition of the malignant phenotype (1). At the core of the metastatic process are the reciprocal interactions between the tumor cells and their microenvironment, as mediated by direct cell-cell contact or cytokine and growth factor signaling. The complexity of the crosstalk among tumor cells, stromal cells, and immune cells determines the response of the host microenvironment, which in turn modifies the invasive behavior of tumor cells. During metastasis, cells leave their “familiar neighborhoods” and in “foreign territory” they rely on interactions with extracellular matrix (ECM) to sense their surroundings (2). The ECM is a dynamic environment, varying from tissue to tissue, as well as at different times and states within a single tissue. The interaction of heterodimeric cell-surface receptors called integrins with the ECM transduces signals between the cells and the ECM (Figure 1). These matrix-initiated signals profoundly affect many cellular functions, including cell survival, proliferation, polarity, motility, differentiation, and even cell proliferation vs survival (3). Cancer cells have the ability to switch the types of integrins they express in order to overcome death signals and to activate pro-survival pathways (4); such resistance to apoptotic signals represents an important aspect of tumor progression, metastasis, and resistance to chemotherapy. Viewpoint