On the orientability of shapes

The orientation of a shape is a useful quantity, and has been shown to affect performance of object recognition in the human visual system. Shape orientation has also been used in computer vision to provide a properly oriented frame of reference, which can aid recognition. However, for certain shapes, the standard moment-based method of orientation estimation fails. We introduce as a new shape feature shape orientability, which defines the degree to which a shape has distinct (but not necessarily unique) orientation. A new method is described for measuring shape orientability, and has several desirable properties. In particular, unlike the standard moment-based measure of elongation, it is able to differentiate between the varying levels of orientability of n-fold rotationally symmetric shapes. Moreover, the new orientability measure is simple and efficient to compute (for an n-gon we describe an O(n) algorithm

CRL4A-FBXW5-mediated degradation of DLC1 Rho GTPase-activating protein tumor suppressor promotes non-small cell lung cancer cell growth

DLC1 encodes a RhoA GTPase-activating protein and tumor suppressor lost in cancer by genomic deletion or epigenetic silencing and loss of DLC1 gene transcription. We unexpectedly identified non-small cell lung cancer (NSCLC) cell lines and tumor tissue that expressed DLC1 mRNA yet lacked DLC1 protein expression. We determined that DLC1 was ubiquitinated and degraded by cullin 4A–RING ubiquitin ligase (CRL4A) complex interaction with DDB1 and the FBXW5 substrate receptor. siRNA-mediated suppression of cullin 4A, DDB1, or FBXW5 expression restored DLC1 protein expression in NSCLC cell lines. FBXW5 suppression-induced DLC1 reexpression was associated with a reduction in the levels of activated RhoA-GTP and in RhoA effector signaling. Finally, FBXW5 suppression caused a DLC1-dependent decrease in NSCLC anchorage-dependent and -independent proliferation. In summary, we identify a posttranslational mechanism for loss of DLC1 and a linkage between CRL4A-FBXW5–associated oncogenesis and regulation of RhoA signaling