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Autophagy is a membrane-trafficking process that delivers cytoplasmic constituents to lysosomes for degradation. It contributes to energy and organelle homeostasis and the preservation of proteome and genome integrity. Although a role in cancer is unquestionable, there are conflicting reports that autophagy can be both oncogenic and tumor suppressive, perhaps indicating that autophagy has different roles at different stages of tumor development. In this report, we address the role of autophagy in a critical stage of cancer progression—tumor cell invasion. Using a glioma cell line containing an inducible shRNA that targets the essential autophagy gene Atg12, we show that autophagy inhibition does not affect cell viability, proliferation or migration but significantly reduces cellular invasion in a 3D organotypic model. These data indicate that autophagy may play a critical role in the benign to malignant transition that is also central to the initiation of metastasis.

The opportunistic pathogen Staphylococcus epidermidis colonizes indwelling medical devices by biofilm formation but is primarily a skin resident. In many S. epidermidis strains biofilm formation is mediated by a cell wall-anchored protein, the accumulation-associated protein (Aap) Staphylococcus epidermidis is the leading cause of nosocomial infections associated with indwelling medical devices including intravascular catheters, cardiac pacemakers, and artificial joints (16,46). The main virulence mechanism is biofilm formation, which promotes persistence in the host, leading to infections such as bacteremia or endocarditis (1). S. epidermidis is also a common commensal resident on the skin all over the human body and may be a transient member of the oral microflora (31, 38). Clinical evidence shows that commensal strains from the skin and mucous membranes can translocate to cause bacteremia (12). In addition, there have been recent reports of linezolid resistance in skin-commensal strains of S. epidermidis (33,41). It is therefore important to study the bacterial factors involved in S. epidermidis colonization of the skin, as this is likely to provide a reservoir for contaminating medical devices..Very little is known about how S. epidermidis colonizes the skin, although many cell wall-associated adhesins that are involved with adhesion, mainly to host matrix proteins, have been identified. The S. epidermidis RP62A genome contains 11 putative LPXTG cell wall-anchored proteins (4), a class of proteins common on gram-positive cocci that often mediate adhesion to host proteins (49). So far, only three of these have prescribed functions: the Bap homology protein (Bhp) and the accumulation-associated protein (Aap) are involved in biofilm formation (13,30,45), and SdrG mediates adhesion to fibrinogen. In addition, S. epidermidis is known to express a variety of other non-LPXTG proteins such as the autolysins Aae, which promotes adhesion to vitronectin and the ␤-chain of fibrinogen (26, 47), and AltE, which promotes adhesion to vitronectin (25). Elastin binding protein (Ebp) (40, 59), extracellular lipase (GehD) (5), extracellular matrix binding protein (Embp) (57), and staphylococcal surface protein 1 (Ssp-1) and Ssp-2 (53) mediate adhesion to elastin, collagen, fibronectin, and polystyrene, respectively. Furthermore, teichoic acids have been shown to promote adhesion to fibronectin (29), and a polysaccharide termed PS/A or PIA (35) promotes adhesion to a plastic used to make catheters (52). To date, no work has been published linking any of these adhesins to the colonization of the skin.We recently showed that one of the LPXTG cell wall-an-* Corresponding author. Mailing address:

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