<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Totonji S</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>University of Freiburg</funding><pagination>1532</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11049522</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(8)</volume><pubmed_abstract>Novel treatment modalities are imperative for the challenging management of muscle-invasive and metastatic BC to improve patient survival rates. The recently identified KMT9, an obligate heterodimer composed of KMT9α and KMT9β, regulates the growth of various types of tumors such as prostate, lung, and colon cancer. While the overexpression of KMT9α was previously observed to be associated with aggressive basal-like MIBC in an analysis of patients' tissue samples, a potential functional role of KMT9 in this type of cancer has not been investigated to date. In this study, we show that KMT9 regulates proliferation, migration, and invasion of various MIBC cell lines with different genetic mutations. KMT9α depletion results in the differential expression of genes regulating the cell cycle, cel</pubmed_abstract><journal>Cancers</journal><pubmed_title>Lysine Methyltransferase 9 (KMT9) Is an Actionable Target in Muscle-Invasive Bladder Cancer.</pubmed_title><pmcid>PMC11049522</pmcid><funding_grant_id>Schu688/15-1, and Schu688/18-1, SFB 992 (Project-ID: 192904750), UcarE and CIBBS Germany ́s Excellence Strategy - EXC-2189 - Project ID: 390939984</funding_grant_id><funding_grant_id>MOTI-VATE Program for Medical Scientists, Faculty of Medicine</funding_grant_id><funding_grant_id>DKTK FR01-374</funding_grant_id><pubmed_authors>Sum M</pubmed_authors><pubmed_authors>Ramos-Triguero A</pubmed_authors><pubmed_authors>Metzger E</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Totonji S</pubmed_authors><pubmed_authors>Urban S</pubmed_authors><pubmed_authors>Bauer H</pubmed_authors><pubmed_authors>Willmann D</pubmed_authors><pubmed_authors>Rieder A</pubmed_authors><pubmed_authors>Greschik H</pubmed_authors><pubmed_authors>Schule R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lysine Methyltransferase 9 (KMT9) Is an Actionable Target in Muscle-Invasive Bladder Cancer.</name><description>Novel treatment modalities are imperative for the challenging management of muscle-invasive and metastatic BC to improve patient survival rates. The recently identified KMT9, an obligate heterodimer composed of KMT9α and KMT9β, regulates the growth of various types of tumors such as prostate, lung, and colon cancer. While the overexpression of KMT9α was previously observed to be associated with aggressive basal-like MIBC in an analysis of patients' tissue samples, a potential functional role of KMT9 in this type of cancer has not been investigated to date. In this study, we show that KMT9 regulates proliferation, migration, and invasion of various MIBC cell lines with different genetic mutations. KMT9α depletion results in the differential expression of genes regulating the cell cycle, cel</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-04-15T03:21:11.106Z</modification><creation>2026-04-15T03:15:13.154Z</creation></dates><accession>S-EPMC11049522</accession><cross_references><pubmed>38672614</pubmed><doi>10.3390/cancers16081532</doi></cross_references></HashMap>