Prevention of metastasis growth presents an unmet clinical need. Anti-angiogenic therapy might provide an alternative way to manipulate cancer, yet it did not materialize into clinical practice. Therefore, combination of anti-angiogenic therapy with cytotoxic therapy directed to the metastatic cancer cells, offers a promising therapeutic approach. Paclitaxel (PTX) is a widely-used potent cytotoxic drug, however, its use is limited by severe side effects, caused by the hydrophobic drug and its solubilizing agents.
We designed and synthesized a novel polyglutamic acid (PGA)-PTX-E-[c(RGDfK)2] nanoconjugate. Polymer conjugation converted PTX to a water-soluble macromolecule, which passively targeted the tumor tissue exploiting the enhanced permeability and retention (EPR) effect, while extravasating via the leaky tumor neovasculature. PGA is enzymatically-degradable by cathepsin B, leading to PTX release. The E-[c(RGDfK)2] serves as an active targeting to αvβ3 integrin. Integrins play a key role in cell matrix interactions. The highly restricted integrin αvβ3 is overexpressed on tumor endothelial and some epithelial cells, during tumor growth, invasion, and metastasis. PGA-PTX-E-[c(RGDfK)2] displayed a potent anti-angiogenic therapy. Mice bearing orthotopic mammary tumors demonstrated preferential tumor accumulation of the RGD-bearing conjugate, leading to enhanced antitumor efficacy and a marked decrease in toxicity compared with free PTX[1].
We used a mouse model that mimics the clinical setting, of mammary cancer metastases following resection of the primary tumor. Integrin αvβ3 expression was detected on circulating mCherry-labeled cancer cells of mice. Adguvant treatment with PGA-PTX-E-[c(RGDfK)2] conjugate prevented metastases formation.
Taken together, our conjugate alters the pharmacokinetics of free PTX. Inclusion of an active targeting moiety to integrin expressing-cells, have the potential to prevent breast cancer metastasis development as an anti-angiogenic and anticancer adjuvant therapy.