{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T21:19:54Z","timestamp":1792790394370,"version":"4.5.0"},"posted":{"date-parts":[[2026,9,18]]},"group-title":"Cancer Biology","reference-count":53,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"name":"National Cancer Institute","award":["1F31CA31406801"],"award-info":[{"award-number":["1F31CA31406801"]}]},{"name":"National Cancer Institute","award":["R37CA258346"],"award-info":[{"award-number":["R37CA258346"]}]},{"name":"National Cancer Institute","award":["P50CA269022"],"award-info":[{"award-number":["P50CA269022"]}]},{"name":"National Cancer Institute","award":["P30CA046592"],"award-info":[{"award-number":["P30CA046592"]}]},{"award":["R01NS129123"],"award-info":[{"award-number":["R01NS129123"]}],"id":[{"id":"https:\/\/ror.org\/01s5ya894","id-type":"ROR","asserted-by":"publisher"}]},{"name":"UMMS Pandemic Research Recovery Program","award":["U083054"],"award-info":[{"award-number":["U083054"]}]},{"name":"Rogel Cancer Center Discovery Award","id":[{"id":"https:\/\/ror.org\/05asdy483","id-type":"ROR","asserted-by":"crossref"}]},{"name":"Michigan Radiosensitization SPORE Career Enhancement Program","award":["5-P50-CA-269022-02"],"award-info":[{"award-number":["5-P50-CA-269022-02"]}]},{"name":"NSF GRFP","award":["DGE2241144"],"award-info":[{"award-number":["DGE2241144"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,9,18]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Radiation therapy (RT) resistance remains a major clinical challenge, yet biomarkers guiding precision radiosensitization are lacking. We previously demonstrated that Rac1 promotes RT resistance in glioblastoma (GBM) by inducing Abi-1-S323 dephosphorylation and enhancing non-homologous end joining (NHEJ). Here, we identify Abi-1-S323 as a key regulator of DNA repair states and a determinant of therapeutic efficacy in human cancers. Clinically, loss of Abi-1-S323 phosphorylation was associated with poor outcomes in patients with RT-treated GBM. Bioinformatic analyses revealed that non-small cell lung cancer (NSCLC) and head and neck cancer (HNC) are among the cancers with frequent\n                  <jats:italic>RAC1<\/jats:italic>\n                  amplification, suggesting that these tumor types may have increased Rac1-Abi-1 signaling activity. Loss of Abi-1-S323 phosphorylation also predicted poor outcomes in patients with RT-treated HNC. Consistent with these clinical observations, high Rac1 activity and low Abi-1-S323 phosphorylation were associated with enhanced DNA double-strand break repair and radioresistance in NSCLC and HNC models, whereas genetic or pharmacological inhibition of this signaling impaired DNA repair and radiosensitized tumors\n                  <jats:italic>in vitro<\/jats:italic>\n                  and\n                  <jats:italic>in vivo<\/jats:italic>\n                  . Mechanistically, we identified CHK1 as a kinase that phosphorylates Abi-1 at S323 and defines an alternative homologous recombination (HR)-dependent repair state. Tumors with high Rac1-Abi-1 signaling exhibited elevated NHEJ capacity and were selectively radiosensitized by Rac1 inhibition, whereas tumors with low Rac1-Abi-1 signaling displayed high CHK1 activity, preferentially relied on HR, and were selectively radiosensitized by CHK1 inhibition. These findings establish Abi-1-S323 as a biomarker defining therapeutically distinct DNA repair states and provide a framework for precision radiosensitization.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Significance<\/jats:title>\n                  <jats:p>Radiation resistance remains a major barrier to cancer treatment. We identify Abi-1-S323 phosphorylation as a biomarker of distinct DNA repair states and therapeutic vulnerabilities, providing a framework for precision radiosensitization.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.09.11.750952","type":"posted-content","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T14:55:29Z","timestamp":1789743329000},"source":"Crossref","is-referenced-by-count":0,"title":["Rac1 and CHK1 Converge on Abi-1 to Regulate DNA Repair Dependency and Treatment Response in Human Cancers"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7277-5054","authenticated-orcid":false,"given":"Yiheng","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Radiation Oncology, University of Michigan, Ann Arbor, 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Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy","family":"Jho","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelica","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kari","family":"Wilder-Romans","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luke 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