ArticleAmerican journal of translational research2026
HORMAD1 inhibits senescence and promotes proliferation of triple negative breast cancer by facilitating ubiquitination-mediated degradation of p27.
Article in American journal of translational research, 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
objectiveTo investigate the role of the HORMA domain containing protein (HORMAD1) in senescence of triple negative breast cancer (TNBC) cells.
methodsWe measured the levels of HORMAD1 and p27 mRNA levels and protein levels in TNBC cell lines using quantitative real -time polymerase chain reaction (PCR) and western blot respectively. We also used the cell counting kit-8 (CCK-8), flow cytometry assays to assess cell viability, cell cycle, apoptosis, immunofluorescence, and co-Immunoprecipitation, respectively.
resultsWe report for the first time that the depletion of HORMAD1 induces cellular senescence through the accumulation of p27 in -TNBC. The increased expression of p27 in HORMAD1-depleted cells was attributed to an impairment of the ubiquitin-mediated degradation of p27. In addition, ectopic expression of HORMAD1 blocked senescence caused by p27 accumulation, which was paralleled by an increase in the growth of TNBC cells. These findings indicate that the impairment of TNBC cell growth is caused by HORMAD1 depletion-induced senescence.
conclusionOur findings suggest that downregulating HORMAD1 expression could serve as a strategy for restricting TNBC progression by inducing senescence by the p27 pathway.
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