<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319983/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type> Methylation profiling by high throughput sequencing</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319983</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Targeted RNA N6-Methyladenosine Demethylation inhibits cell migration in colorectal cancer cells [MeRIP-seq]</name><description>Colorectal cancer liver metastasis (CRLM) remains a significant challenge in the treatment of colorectal cancer (CRC). N6-methyladenosine (m6A) as a new layer of epigenetic RNA modification is closely linked to various mechanisms of tumor metastasis, offering new avenues for targeted therapies. However, the role of m6A-mediated mechanisms underlying colorectal liver metastasis is still unclear. In this study, we identified a novel m6A-modified transcriptional factor BTB/POZ domain protein ZBTB7A (zinc finger and BTB domain-containing 7A) using integrative m6A-sequencing (MeRIP-seq), RNA sequencing (RNA-seq), and single-cell RNA sequencing (scRNA-seq) analyses, and investigated the functional signiﬁcance and underlying mechanisms of ZBTB7A as a promoting factor in liver metastasis of CRC. Mechanically, ZBTB7A could be positively regulated by m6A methyltransferase METTL3 and promote the process of CRLM through ARHGAP26-mediated Rho GTPases signaling pathway in a m6A-dependent manner. More importantly, we also applied a targeted RNA m6A erasure (TRME) system to focus methylation on a specific site within a transcript of interest rather altering global levels of m6A abundance and demonstrated that temporal m6A erasure on a single site of ZBTB7A is suﬃcient to inhibit the CRC cell migration. This study unveils the critical role of the METTL3/ZBTB7A/ARHGAP26 axis in the process of m6A-mediated CRLM and positions m6A precise editing as a promising therapy in the preclinical treatment of tumor metastasis.</description><dates><publication>2026/09/02</publication></dates><accession>GSE319983</accession><cross_references><GSM>GSM9530804</GSM><GSM>GSM9530805</GSM><GSM>GSM9530802</GSM><GSM>GSM9530803</GSM><GSM>GSM9530806</GSM><GSM>GSM9530807</GSM><GSM>GSM9093379</GSM><GSM>GSM9093378</GSM><GSM>GSM9093377</GSM><GSM>GSM9093376</GSM><GSM>GSM9093375</GSM><GSM>GSM9093374</GSM><GSM>GSM9093373</GSM><GSM>GSM9093383</GSM><GSM>GSM9093372</GSM><GSM>GSM9093382</GSM><GSM>GSM9093381</GSM><GSM>GSM9093380</GSM><GPL>24676</GPL><GSE>319983</GSE><taxon>Homo sapiens</taxon><PMID>[42649501]</PMID></cross_references></HashMap>