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Inhibitor of growth protein 5 (ING5) is a member of the ING tumor suppressor family, encoded on human chromosome 2q37.3, with a typical structure comprising a plant homeodomain (PHD), nuclear localization signal (NLS), novel conserved region (NCR), and leucine zipper-like (LZL) domains[2][4]. ING5 forms both homodimers and heterodimers, interacting with chromatin and regulatory protein complexes, notably histone acetyltransferase (HAT) assemblies like MOZ/MORF and HBO1[1][2][3]. ING5 functions as an epigenetic reader and cofactor that recognizes histone H3K4 methylation marks and facilitates the acetylation of histones and proteins such as p53, thereby controlling gene transcription, cell cycle arrest, and apoptosis. ING5’s tumor suppressive activities are exerted via p53 acetylation and p21 activation, inhibiting colony formation and promoting apoptosis[1][2][3][5][6]. In cancer, ING5 suppresses cell proliferation, invasion, migration, and induces autophagy, senescence, and cell death through modulation of diverse signaling pathways (EGFR/Akt/NF-κB, IL-6/STAT3, Wnt/β-catenin, etc.), and its deficiency or cytoplasmic relocalization is linked to poor prognosis and chemoresistance[3][4][6]. ING5 is also implicated in the regulation of stem cell populations and metabolic processes, including lipogenesis, making it a potential target for cancer and metabolic disease therapy[3][4].
Not applicable (no direct therapeutic drugs)—experimental strategies include gene therapy, gene knockout, and pathway suppression to modulate its tumor suppressor or metabolic effects[3][4]. In some contexts, "anti-ING5 reagents" are suggested as potential therapies to reverse chemoresistance and control obesity[3].
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