<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang S</submitter><funding>HMRF</funding><pagination>344</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5437682</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>DNA repair pathways are used by cancer cells to overcome many standard anticancer treatments, causing therapy resistance. Here, we investigated the role of XRCC4-like factor (XLF), a core member of the non-homologous end joining (NHEJ) repair pathway, in chemoresistance in hepatocellular carcinoma (HCC).&lt;h4>Methods&lt;/h4>qRT-PCR analysis and western blotting were performed to detect expression levels of genes and proteins related to NHEJ. NHEJ repair capacity was assessed in vitro (cell-free) and in vivo by monitoring the activity of the NHEJ pathway. Cell viability and IC50 assays were used to measure sensitivity to drug therapy. A xenograft HCC model was used to develop methods of targeting XLF-induced chemosensitization. Clinicopathological analysis was conducted on pat</pubmed_abstract><journal>BMC cancer</journal><pubmed_title>XLF-mediated NHEJ activity in hepatocellular carcinoma therapy resistance.</pubmed_title><pmcid>PMC5437682</pmcid><funding_grant_id>03143396</funding_grant_id><pubmed_authors>Wang XQ</pubmed_authors><pubmed_authors>Yang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>XLF-mediated NHEJ activity in hepatocellular carcinoma therapy resistance.</name><description>&lt;h4>Background&lt;/h4>DNA repair pathways are used by cancer cells to overcome many standard anticancer treatments, causing therapy resistance. Here, we investigated the role of XRCC4-like factor (XLF), a core member of the non-homologous end joining (NHEJ) repair pathway, in chemoresistance in hepatocellular carcinoma (HCC).&lt;h4>Methods&lt;/h4>qRT-PCR analysis and western blotting were performed to detect expression levels of genes and proteins related to NHEJ. NHEJ repair capacity was assessed in vitro (cell-free) and in vivo by monitoring the activity of the NHEJ pathway. Cell viability and IC50 assays were used to measure sensitivity to drug therapy. A xenograft HCC model was used to develop methods of targeting XLF-induced chemosensitization. Clinicopathological analysis was conducted on pat</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 May</publication><modification>2025-04-19T19:07:00.229Z</modification><creation>2019-03-27T02:45:26Z</creation></dates><accession>S-EPMC5437682</accession><cross_references><pubmed>28526069</pubmed><doi>10.1186/s12885-017-3345-y</doi></cross_references></HashMap>