In Drosophila, the adult thoracic Air Sacs supply oxygen to the flight muscles. These Air Sacs develop from a group of larval cells that form the Air Sac Primordium (ASP). The ASP is located superficially over the larval wing imaginal disc and in response to Fibroblast Growth Factor (FGF) signal, migrates and invades into the wing imaginal disc to occupy a more deep seated position. The regulation of invasive behavior during ASP development is not well understood. Data are presented that implicate a Cathepsin-L in ASP development and invasive cellular behavior. Utilizing immunohistochemistry and confocal microscopy we assessed the expression of Cathepsin-L in larval wing imaginal discs. The knockdown of Cathepsin-L in ASP was achieved by UAS-Gal4 driven RNAi and the overexpression of Cathepsin-L was performed using the UAS-Gal4 system of gene expression in Drosophila. We found that a single Cathepsin-L is upregulated in the ASP and downregulation of this gene results in aberrant ASP development, loss of Filopodia from ASP and suppression of invasive behavior. Furthermore, we demonstrate that overexpression of Cathepsin-L results in degradation of the Basement Membrane (BM). Our data demonstrate that a Cathepsin-L is involved in the development of ASP by regulating the invasive cellular behavior and by degrading the BM. These data are particularly significant given that Cathepsin-L is also expressed during early human lung development and invasive cellular behavior and degradation of the BM are critical events during tumor metastasis.