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HMGA1P7 is a processed pseudogene and lncRNA, located on chromosome 6q23.2, that shares high sequence homology with the parental HMGA1 gene but cannot be translated into functional protein due to a mutation in the initiator methionine codon. Instead, HMGA1P7 regulates gene expression post-transcriptionally by competing endogenous RNA (ceRNA) activity: it sequesters microRNAs that target the HMGA1 gene and other cancer-related genes such as HMGA2, EZH2, and VEGF, thereby upregulating their expression. Overexpression of HMGA1P7 has been associated with increased cellular proliferation, decreased apoptosis, enhanced migration and invasion, and higher tumor aggressiveness in both cellular and animal models. In transgenic mice, overexpression causes hematological neoplasia, notably diffuse large B-cell lymphoma, providing functional evidence of its oncogenic potential in vivo. As such, HMGA1P7 is an important regulator in cancer biology, despite not being a typical therapeutic target or druggable protein.
Not applicable. No agents are known to act directly on HMGA1P7. Its biological effect is mediated by acting as a microRNA "sponge," sequestering microRNAs that would otherwise repress key oncogenes.
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