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Fig. 8 | Molecular Cancer

Fig. 8

From: The tumor suppressor activity of DLC1 requires the interaction of its START domain with Phosphatidylserine, PLCD1, and Caveolin-1

Fig. 8

Simplified graphical summary of working hypothesis. A Under low phosphatidylserine (PS) conditions, most DLC1 is present in the cytosolic compartment. The pool of DLC1 in the membrane (if any) may bind the existing Caveolin-1 (Cav1), or Phospholipase C delta 1 (PLCD1), although we hypothesize that this binding is weak. B High PS levels promotes the recruitment of DLC1 to the membrane. B1). At high PS levels, Cav1 presence in the membrane is higher, and the membrane-recruited DLC1 interacts more efficiently to the existing Cav1. Therefore, DLC1 inhibition of tumorigenesis (migration, anchorage-independent growth) is stronger. B2). When PLCD1 levels are increased, more PLCD1 is recruited to the membrane. Competition between PLCD1 and Cav1 for DLC1 binding exists, displacing the DLC1/Cav1 interaction. DLC1 inhibition of tumorigenesis is still strong. Not represented: At low PS, there is still competition between Cav1 or PLCD1 to bind DLC1. At high PS levels and high PLCD1 levels, Cav1 still binds PS, but at other regions of the membrane where PLCD1 is not binding

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