<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lin Y</submitter><funding>the Natural Science Foundation of Fujian Province</funding><funding>the Young and Middle-aged Backbone Research Fund of Fujian Provincial Health Care Commission</funding><funding>National Natural Science Foundation of China</funding><funding>Startup Fund for scientific research, Fujian Medical University</funding><funding>Fujian Provincial Medical Science and Technology Innovation Joint Fund Project</funding><pagination>1</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10759737</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Ceramide metabolism is crucial in the progress of brain metastasis (BM). However, it remains unexplored whether targeting ceramide metabolism may arrest BM.&lt;h4>Methods&lt;/h4>RNA sequencing was applied to screen different genes in primary and metastatic foci and whole-exome sequencing (WES) to seek crucial abnormal pathway in BM + and BM-patients. Cellular arrays were applied to analyze the permeability of blood-brain barrier (BBB) and the activation or inhibition of pathway. Database and Co-Immunoprecipitation (Co-IP) assay were adopted to verify the protein-protein interaction. Xenograft and zebrafish model were further employed to verify the cellular results.&lt;h4>Results&lt;/h4>RNA sequencing and WES reported the involvement of RPTOR and ceramide metabolism in BM progress. R</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>RPTOR blockade suppresses brain metastases of NSCLC by interfering the ceramide metabolism via hijacking YY1 binding.</pubmed_title><pmcid>PMC10759737</pmcid><funding_grant_id>2020J011106</funding_grant_id><funding_grant_id>2018QH1130</funding_grant_id><funding_grant_id>2020Y9023</funding_grant_id><funding_grant_id>82002457</funding_grant_id><funding_grant_id>2019-ZQNB-1</funding_grant_id><funding_grant_id>2020GGA010</funding_grant_id><funding_grant_id>2013J011177</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Pan J</pubmed_authors><pubmed_authors>Xu N</pubmed_authors><pubmed_authors>She P</pubmed_authors><pubmed_authors>Lin Y</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Chen S</pubmed_authors><pubmed_authors>Niu G</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Zhang Q</pubmed_authors><pubmed_authors>Tu X</pubmed_authors><pubmed_authors>Lin M</pubmed_authors></additional><is_claimable>false</is_claimable><name>RPTOR blockade suppresses brain metastases of NSCLC by interfering the ceramide metabolism via hijacking YY1 binding.</name><description>&lt;h4>Background&lt;/h4>Ceramide metabolism is crucial in the progress of brain metastasis (BM). However, it remains unexplored whether targeting ceramide metabolism may arrest BM.&lt;h4>Methods&lt;/h4>RNA sequencing was applied to screen different genes in primary and metastatic foci and whole-exome sequencing (WES) to seek crucial abnormal pathway in BM + and BM-patients. Cellular arrays were applied to analyze the permeability of blood-brain barrier (BBB) and the activation or inhibition of pathway. Database and Co-Immunoprecipitation (Co-IP) assay were adopted to verify the protein-protein interaction. Xenograft and zebrafish model were further employed to verify the cellular results.&lt;h4>Results&lt;/h4>RNA sequencing and WES reported the involvement of RPTOR and ceramide metabolism in BM progress. R</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jan</publication><modification>2025-04-04T14:43:21.735Z</modification><creation>2024-11-20T22:55:06.25Z</creation></dates><accession>S-EPMC10759737</accession><cross_references><pubmed>38163890</pubmed><doi>10.1186/s13046-023-02874-z</doi></cross_references></HashMap>