<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yoshida M</submitter><funding>Japan Agency for Medical Research and Development</funding><funding>Japan Society for the Promotion of Science</funding><pagination>8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9847160</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Antisense oligonucleotide (ASO) medicine for clinical applications has been becoming a reality. We previously developed a gapmer ASO targeting Ser/Arg repetitive matrix 4 (SRRM4) that is abnormally expressed in small cell lung cancer (SCLC). However the detailed mechanism of ASO through repressing SRRM4 has not been completely elucidated. Further, effectiveness of SRRM4 ASO to prostate cancer (PCa) cells expressing SRRM4 similar to SCLC remains to be elucidated. RE1-silencing transcription factor (REST) is a tumor suppressor, and its splicing isoform (sREST) is abnormally expressed by SRRM4 and causes carcinogenesis with neuroendocrine phenotype in SCLC. The present study aimed to understand the contribution of REST splicing by SRRM4 ASO administration.&lt;h4>Methods&lt;/h4>SR</pubmed_abstract><journal>Cancer cell international</journal><pubmed_title>An antisense amido-bridged nucleic acid gapmer oligonucleotide targeting SRRM4 alters REST splicing and exhibits anti-tumor effects in small cell lung cancer and prostate cancer cells.</pubmed_title><pmcid>PMC9847160</pmcid><funding_grant_id>22K07230</funding_grant_id><funding_grant_id>JP22am0401003</funding_grant_id><pubmed_authors>Yoshida M</pubmed_authors><pubmed_authors>Tsuji I</pubmed_authors><pubmed_authors>Oda C</pubmed_authors><pubmed_authors>Mishima K</pubmed_authors><pubmed_authors>Shimojo M</pubmed_authors><pubmed_authors>Obika S</pubmed_authors></additional><is_claimable>false</is_claimable><name>An antisense amido-bridged nucleic acid gapmer oligonucleotide targeting SRRM4 alters REST splicing and exhibits anti-tumor effects in small cell lung cancer and prostate cancer cells.</name><description>&lt;h4>Background&lt;/h4>Antisense oligonucleotide (ASO) medicine for clinical applications has been becoming a reality. We previously developed a gapmer ASO targeting Ser/Arg repetitive matrix 4 (SRRM4) that is abnormally expressed in small cell lung cancer (SCLC). However the detailed mechanism of ASO through repressing SRRM4 has not been completely elucidated. Further, effectiveness of SRRM4 ASO to prostate cancer (PCa) cells expressing SRRM4 similar to SCLC remains to be elucidated. RE1-silencing transcription factor (REST) is a tumor suppressor, and its splicing isoform (sREST) is abnormally expressed by SRRM4 and causes carcinogenesis with neuroendocrine phenotype in SCLC. The present study aimed to understand the contribution of REST splicing by SRRM4 ASO administration.&lt;h4>Methods&lt;/h4>SR</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T14:27:56.663Z</modification><creation>2025-02-19T03:30:25.574Z</creation></dates><accession>S-EPMC9847160</accession><cross_references><pubmed>36650528</pubmed><doi>10.1186/s12935-022-02842-1</doi></cross_references></HashMap>