VIM and cancer: As the knockdown of plectin in cancer cells severely impaired their potential to form invadopodia and reduced their capacities of extracellular matrix degradation, transendothelial migration, and metastasis, it was suggested that plectin-mediated crosslinking of vimentin scaffolds to actin stabilizes invadopodia and promotes their extension, which is critical for cancer cell invasion and extravasation for metastasis [81].