<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lian Q</submitter><funding>the Fujian Provincial Clinical Medical Research Center for First Aid and Rehabilitation in Orthopedic Trauma</funding><funding>the Youth Cultivation Program for Medical-Engineering Interdisciplinary Research at the Third Affiliated Hospital of Naval Medical University</funding><funding>the National Natural Science Foundation of China</funding><pagination>159</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12102912</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>44(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The prognosis of osteosarcoma has improved little over the past few decades, with radioresistance being a contributing factor. Effective radiosensitizing targets and novel mechanisms for treating osteosarcoma are urgently needed. Research on the impact of regulating differentiation levels on the radiosensitivity of malignant tumors is limited. This study aimed to explore the efficacy of ITGB3 as a novel radiosensitizing target in osteosarcoma and to explore whether the modulation of osteogenic differentiation plays a role in mediating the radiosensitizing effect.&lt;h4>Methods&lt;/h4>RNA sequencing was utilized to screen for potential targets that affect the radiosensitivity of osteosarcoma. In vitro assays examining cell viability, apoptosis, proliferation, migration, and inv</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.</pubmed_title><pmcid>PMC12102912</pmcid><funding_grant_id>2022YGJC003</funding_grant_id><funding_grant_id>82171383</funding_grant_id><funding_grant_id>2020Y2014</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Qiao S</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Dai P</pubmed_authors><pubmed_authors>Jiang X</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Luo C</pubmed_authors><pubmed_authors>Zhou H</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Lian Q</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.</name><description>&lt;h4>Background&lt;/h4>The prognosis of osteosarcoma has improved little over the past few decades, with radioresistance being a contributing factor. Effective radiosensitizing targets and novel mechanisms for treating osteosarcoma are urgently needed. Research on the impact of regulating differentiation levels on the radiosensitivity of malignant tumors is limited. This study aimed to explore the efficacy of ITGB3 as a novel radiosensitizing target in osteosarcoma and to explore whether the modulation of osteogenic differentiation plays a role in mediating the radiosensitizing effect.&lt;h4>Methods&lt;/h4>RNA sequencing was utilized to screen for potential targets that affect the radiosensitivity of osteosarcoma. In vitro assays examining cell viability, apoptosis, proliferation, migration, and inv</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 May</publication><modification>2026-07-15T12:36:51.252Z</modification><creation>2026-07-04T03:14:14.097Z</creation></dates><accession>S-EPMC12102912</accession><cross_references><pubmed>40410897</pubmed><doi>10.1186/s13046-025-03417-4</doi></cross_references></HashMap>