Integrin subunit beta 4 (ITGB4) (ITGB4)

Integrin subunit beta 4 (ITGB4) is a critical transmembrane protein that pairs with the alpha-6 subunit to form the alpha-6-beta-4 integrin, a primary receptor for laminins in epithelial tissues [1, 5]. Unlike other integrins, ITGB4 features an exceptionally long cytoplasmic tail that links the extracellular matrix to the intermediate filament (keratin) cytoskeleton, facilitating the formation of hemidesmosomes [1, 2]. In various malignancies, including triple-negative breast cancer and lung adenocarcinoma, ITGB4 mRNA is significantly upregulated, where it drives tumor progression by activating pro-survival and migratory signaling pathways such as PI3K/Akt and Src [3, 4]. Targeting ITGB4 mRNA through RNA interference (RNAi) or antisense oligonucleotides (ASOs) represents a therapeutic strategy to deplete the protein pool and inhibit metastasis [4]. However, because ITGB4 is essential for maintaining the structural integrity of the dermo-epidermal junction, its inhibition poses risks of severe skin blistering and mucosal erosions, similar to the phenotype seen in junctional epidermolysis bullosa [1, 5]. Consequently, therapeutic development must balance potent tumor suppression with the preservation of normal epithelial adhesion [3]. Sources: [1] UniProt (P16144) [2] NCBI Gene (3691) [3] PubMed (PMID: 30217958) [4] PubMed (PMID: 25646686) [5] Wikipedia (Integrin beta 4)

Other names

CD104Integrin beta-4GP150ITGB4 mRNA

RNA interference (RNAi) or antisense-mediated degradation of ITGB4 mRNA to prevent the translation and surface expression of the Integrin alpha-6-beta-4 complex, thereby inhibiting pro-tumorigenic signaling and cell adhesion.