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Tetraspanin-induced death of myeloma cell lines is autophagic and involves increased UPR signalling
British Journal of Cancer, 09/17/09

Zismanov V et al. – Multiple myeloma (MM) therapy is hindered by the interaction of the heterogeneous malignant plasma cells with their microenvironment and evolving drug resistance. This is the first publication implicating tetraspanins in UPR signalling pathways, autophagy, and autophagic death. Integration of the findings with published data highlights the unifying dependence of MM cells on ER–Golgi homoeostasis, and underscores the potential of tetraspanin complexes and ER–stress as leverage for MM therapy.

Exclusive Author Commentary
L Drucker, 09/22/09

In our study we demonstrate that autophagy death is achievable in multiple myeloma cell lines. Death was caused as a result of signaling instigated by transfected tetraspanin-fusion-proteins thereby positioning their circuitry upstream of ER-stress and providing evidence of the role of cancer microenvironment in basic cellular functions. Moreover, these results portray protein synthesis machinery as a stress sensing organelle with clinical potential in myeloma therapy. We propose that ER-stress may be achieved by increasing protein synthesis, thus exploiting myeloma cells characteristics as their Achilles' heal and the path of least resistance.

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