{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Prokarenkaite R"],"funding":["Lietuvos Mokslo Taryba","National Cancer Institute","NCI NIH HHS"],"pagination":["199"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12247367"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(1)"],"pubmed_abstract":["Background
Colorectal cancer (CRC) is the third most prevalent cancer worldwide. Despite substantial advancements in CRC therapy in recent years, ionizing radiation (IR) continues to be the predominant treatment for colon malignances. However, it still lacks the precision required for excellent therapeutic outcomes, ultimately resulting in tumor radioresistance. This study seeks to explore the potential of atypical PARPs including PARP9, PARP12, PARP13 and PARP14 as innovative radiosensitizing targets for CRC.Methods
We utilized CRISPR/Cas9-mediated gene editing to knockout the PARP9, PARP12, PARP13 and PARP14 in HT29 and DLD1 cells. The cells were exposed to either a single dose of 6-10 Gy or to fractionated dose of 5 × 2 Gy X-ray radiation cultivating cells in 2D, laminin"],"journal":["Journal of experimental & clinical cancer research : CR"],"pubmed_title":["PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy."],"pmcid":["PMC12247367"],"funding_grant_id":["VP1-3.1-SMM-10-V-02-027","MTEP-2"],"pubmed_authors":["Dulskas A","Stankevicius V","Tunaitis V","Sileika E","Starkuviene V","Budginaite E","Gudoityte G","Velickevicius K","Strainiene E","Kuodyte K","Pivoriunas A","Venius J","Naumovas D","Prokarenkaite R","Suziedelis K"],"additional_accession":[]},"is_claimable":false,"name":"PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy.","description":"Background
Colorectal cancer (CRC) is the third most prevalent cancer worldwide. Despite substantial advancements in CRC therapy in recent years, ionizing radiation (IR) continues to be the predominant treatment for colon malignances. However, it still lacks the precision required for excellent therapeutic outcomes, ultimately resulting in tumor radioresistance. This study seeks to explore the potential of atypical PARPs including PARP9, PARP12, PARP13 and PARP14 as innovative radiosensitizing targets for CRC.Methods
We utilized CRISPR/Cas9-mediated gene editing to knockout the PARP9, PARP12, PARP13 and PARP14 in HT29 and DLD1 cells. The cells were exposed to either a single dose of 6-10 Gy or to fractionated dose of 5 × 2 Gy X-ray radiation cultivating cells in 2D, laminin","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-07-15T14:24:14.783Z","creation":"2026-07-05T03:12:13.199Z"},"accession":"S-EPMC12247367","cross_references":{"pubmed":["40646573"],"doi":["10.1186/s13046-025-03439-y"]}}