{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:57:07Z","timestamp":1790618227926,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:00:00Z","timestamp":1788480000000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004829","name":"Science and Technology Department of Sichuan Province","doi-asserted-by":"publisher","award":["2020JDRC0139"],"award-info":[{"award-number":["2020JDRC0139"]}],"id":[{"id":"10.13039\/501100004829","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Reports"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Glioblastoma (GBM) is a common brain cancer with a poor prognosis and a high recurrence rate. DNA damage repair plays a crucial role in GBM carcinogenesis and treatment resistance. Human endogenous bornavirus\u2010like nucleoprotein 1 (EBLN1) regulates cellular processes and genetic stability. However, the biological role of EBLN1 in GBM remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>This study aims to determine the role of EBLN1 in the regulation of cellular processes and DNA double\u2010strand breaks (DSBs) in GBM and to investigate the underlying molecular mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p>\n                      U\u201087 MG GBM cells were infected with an shRNA\u2010expressing lentivirus to knock down EBLN1. Then, cell proliferation and apoptosis were evaluated. The levels of DSBs, as well as the activities of two key DSB repair regulators\u2014ataxia telangiectasia mutated (ATM) kinase and breast cancer Type 1 susceptibility protein (BRCA1)\u2014were detected. Furthermore, after reactivating ATM, cellular processes and the levels of DSBs were re\u2010detected to verify the mechanisms underlying EBLN1\u2010mediated DNA repair regulation in GBM. EBLN1\u2010silenced U\u201087 MG cells displayed a significant reduction in cell growth as early as the second day postinfection (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05) and a higher apoptosis ratio (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). After EBLN1\u2010silencing, U\u201087 MG cells exhibited a remarkable increase in the expression of \u03b3H2AX (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and significantly lower expression levels of ATM and BRCA1 (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). After reactivation of ATM in EBLN1\u2010silenced U\u201087 MG cells, DSB levels in the treated cells were significantly decreased (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Meanwhile, cell proliferation was significantly increased (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), while apoptosis was markedly suppressed (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study uncovers a novel molecular mechanism that EBLN1 regulates cellular processes via modulating DNA double\u2010strand break repair in glioblastoma cells, providing a new perspective for understanding the pathogenesis of GBM.<\/jats:p>\n                  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