@Article{or.2026.076051,
AUTHOR = {Jun Jiang, Yi-Ran Li, Xiaoting Wang, Jian Li, Fangzhou Ye, Jiayi Wang, Huanqing Li, Li Feng},
TITLE = {<i>CDCA7</i> Promotes Proliferation and Suppresses Apoptosis in Gastric Cancer via HELLS-Mediated Chromatin Remodeling},
JOURNAL = {Oncology Research},
VOLUME = {34},
YEAR = {2026},
NUMBER = {5},
PAGES = {0--0},
URL = {http://www.techscience.com/or/v34n5/67068},
ISSN = {1555-3906},
ABSTRACT = { <b>Background:</b> In various tumor types, cell division cycle-associated 7 (<i>CDCA7</i>) is involved in chromatin remodeling and DNA methylation. However, its biological functions and regulatory mechanisms in gastric cancer (GC) remain unknown. This investigation intended to identify the function of <i>CDCA7</i> in GC progression and elucidate its epigenetic regulatory mechanisms. <b>Methods:</b> Differentially expressed genes (DEGs) were detected from the GSE19826, TCGA-GC, and GSE56807 datasets. Networks of protein-protein interactions (PPI) and hub genes were discovered by the DMNC and Clustering Coefficient algorithms. Receiver operating characteristic (ROC) analysis and expression profiling were undertaken to determine diagnostic performance. <i>In vitro</i> assays, including CCK-8 assays, clonogenic assays, flow cytometry, dot blots, co-immunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), and Western blots, were applied to evaluate the role of <i>CDCA7</i> and its interaction with helicase, lymphoid-specific (<i>HELLS</i>). <b>Results:</b> 169 overlapping genes were discovered, enriched in Cell adhesion molecules and ECM-receptor interaction. <i>CDCA7</i> is highly expressed in GC and has high clinical diagnostic value. Knockdown of <i>CDCA7</i> causes apoptosis and suppresses GC cell invasion, migration, and proliferation. Mechanistically, CDCA7 physically interacts with HELLS and promotes HELLS recruitment to chromatin. Knockdown of <i>CDCA7</i> reduces global 5 hmC/5 mC levels and histone methylation (H3K9me3 and H4K20me3), while <i>HELLS</i> overexpression partially reverses these effects. Functionally, <i>HELLS</i> overexpression also partially reverses the antiproliferative and proapoptotic effects of <i>CDCA7</i> knockdown. <b>Conclusion:</b> <i>CDCA7</i> promotes GC progression by interacting with <i>HELLS</i> to regulate DNA methylation and chromatin stability, suggesting that the <i>CDCA7</i>-<i>HELLS</i> axis may serve as a potential diagnostic biomarker and therapeutic target for GC.},
DOI = {10.32604/or.2026.076051}
}