Saposin C was shown to be a trophic factor for a variety of cancer cells, e.g., prostate, lung, breast, and colon cancer cells. These cells expressed saposin C and responded to saposin C by increased levels of cell proliferation, cell migration, and cell invasion. Such activities typify and promote the neoplastic process. For prostate cancer, the androgen-insensitive prostate cancer cells responded to saposin C by higher levels of cell proliferation, cell migration and cell invasion than did the androgen-sensitive prostate cells. Stromal cells (from the prostate) were also responsive to saposin C-mediated signals in a manner typical of growth promoting compounds. The androgen-insensitive prostate cells were stimulated by saposin C to express higher levels of the urokinase plasminogen activator (uPA) and its receptor (uPAR), two proteins known to be involved in cell invasion. A conjugate of a peptide of the active region of saposin C (TX14A) and a toxin (saporin) was made and was shown to decrease the survival of prostate cancer cells, and the other cancer cells that were found to express saposin C (including cancers cells of the breast, colon, and lung). This conjugate or a compound of analogous action that inhibits cellular growth acting via a saposin-C binding receptor can be used to decrease tumor growth and/or treat disorders of stromal proliferation (e.g., benign prostatic hyperplasia, atherosclerosis, and vascular restenosis).