{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cui X"],"funding":["Breast Cancer Research Foundation of Alabama","Congressionally Directed Medical Research Programs","NCI NIH HHS"],"pagination":["38"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8819949"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<h4>Background</h4>Unlike autosomal tumor suppressors, X-linked tumor suppressors can be inactivated by a single hit due to X-chromosome inactivation (XCI). Here, we argue that targeted reactivation of the non-mutated allele from XCI offers a potential therapy for female breast cancers.<h4>Methods</h4>Towards this goal, we developed a dual CRISPR interference and activation (CRISPRi/a) approach for simultaneously silencing and reactivating multiple X-linked genes using two orthogonal, nuclease-deficient CRISPR/Cas9 (dCas9) proteins.<h4>Results</h4>Using Streptococcus pyogenes dCas9-KRAB for silencing XIST and Staphylococcus aureus dCas9-VPR for activating FOXP3, we achieved CRISPR activation of FOXP3 in various cell lines of human female breast cancers. In human breast cancer HCC202 cells,"],"journal":["Molecular cancer"],"pubmed_title":["Dual CRISPR interference and activation for targeted reactivation of X-linked endogenous FOXP3 in human breast cancer cells."],"pmcid":["PMC8819949"],"funding_grant_id":["P30 CA013148","W81XWH-17-1-0018","W81XWH-17-1-0017"],"pubmed_authors":["Li X","Stringer-Reasor E","Wang S","Bae S","Zeng L","Cui X","Liu R","Qi LS","Zhao D","Zhang C","Xu Z","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Dual CRISPR interference and activation for targeted reactivation of X-linked endogenous FOXP3 in human breast cancer cells.","description":"<h4>Background</h4>Unlike autosomal tumor suppressors, X-linked tumor suppressors can be inactivated by a single hit due to X-chromosome inactivation (XCI). Here, we argue that targeted reactivation of the non-mutated allele from XCI offers a potential therapy for female breast cancers.<h4>Methods</h4>Towards this goal, we developed a dual CRISPR interference and activation (CRISPRi/a) approach for simultaneously silencing and reactivating multiple X-linked genes using two orthogonal, nuclease-deficient CRISPR/Cas9 (dCas9) proteins.<h4>Results</h4>Using Streptococcus pyogenes dCas9-KRAB for silencing XIST and Staphylococcus aureus dCas9-VPR for activating FOXP3, we achieved CRISPR activation of FOXP3 in various cell lines of human female breast cancers. In human breast cancer HCC202 cells,","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-18T16:34:09.128Z","creation":"2024-11-08T11:42:42.996Z"},"accession":"S-EPMC8819949","cross_references":{"pubmed":["35130925"],"doi":["10.1186/s12943-021-01472-x"]}}