Keratin, type I cytoskeletal 23 (KRT23)

Keratin, type I cytoskeletal 23 (KRT23) is an intermediate filament protein primarily responsible for maintaining the structural integrity of epithelial cells[2]. It is a type I (acidic) cytokeratin encoded on human chromosome 17q21.2. KRT23 is typically expressed in epithelial tissues and shows aberrant overexpression in several cancers, including ovarian, colorectal, pancreatic, and liver cancers[1][2][3]. In cancer, KRT23 is implicated in promoting cell proliferation, epithelial-to-mesenchymal transition (EMT), increased cellular migration, invasion, and cancer stem cell traits, partly via modulation of the TGF-β/Smad and MAPK signaling pathways[1][3]. KRT23 can also bind the hTERT promoter, thereby enhancing telomerase expression and activity in malignant contexts[3]. Its pathological overexpression correlates with tumor progression, resistance to DNA damage, and poor prognosis[1][2]. It is experimentally validated as a potential biomarker for tumor progression and as an indicator of disease severity in liver disease; however, no specific therapeutics directly targeting KRT23 are currently available[2][3].

Other names

Keratin 23CK-23K23DKFZP434G032HAIK1CK23MGC26158Cytokeratin-23Keratin-23histone deacetylase inducible keratin 23hyperacetylation-inducible type I keratinkeratin 23 (histone deacetylase inducible)type I intermediate filament cytokeratincytokeratin 23

Not drug-targeted. Experimental knockdown (siRNA) reduces migration and invasion in cancer cells[1][3]. Modulation of TGF-β/Smad signaling pathway and MAPK signaling in cancer cell models[1][3].