ArticleFunctional & integrative genomics2026
HJURP upregulation, driven by transcription factor NFYA, promotes endometrial carcinoma progression via regulating RASSF8 ubiquitination.
Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Endometrial carcinoma (EC) is the most common malignant gynecological cancer with high mortality. Holliday junction recognition protein (HJURP), an E3 ubiquitin ligase dysregulated in various malignancies, has an unclear role in EC. We assessed HJURP's effects on growth, metastasis, and invasion of EC cells in in vivo and in vitro experiments. Proteomics compared protein expression in EC cells with and without HJURP overexpression. Finally, the regulatory network around HJURP was validated using base mutations and immunoprecipitation assays. Data from the clinical samples (n = 47) revealed high expression of HJURP in EC tissues compared with normal tissues. The correlation between HJURP expression and clinicopathology in 94 patients was analyzed, and the results showed that high expression of HJURP was significantly correlated with FIGO stage, tumor stage, and TNM stage (all p < 0.05). Patients with high HJURP expression exhibited significantly lower overall survival and recurrence-free survival rates compared to those with low HJURP expression. Downregulation of HJURP exhibited anti-proliferation and anti-metastasis in vivo and in vitro. Conversely, the forced expression of HJURP had a carcinogenic effect. Notably, HJURP RNA levels were upregulated by transcription factor nuclear factor Y alpha subunit (NFYA). NFYA promoted HJURP transcription by binding to its promoter region. Proteomic analysis showed that HJURP decreased Ras association domain-containing protein 8 (RASSF8) protein level (about 2-fold). Specifically, HJURP may mediate the ubiquitin-dependent degradation of RASSF8 by recruiting E2 or E3 ligases, such as ubiquitin-conjugating enzyme E2O. RASSF8 overexpression weakened the effects of HJURP overexpression. HJURP, transcriptionally activated by NFYA, exerts oncogenic functions via interacting with and destabilizing RASSF8, indicating that HJURP may act as a promising target for EC therapies.
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