<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wu Q</submitter><funding>National Natural Science Foundation of China</funding><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><pagination>582-594</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6294659</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>144(3)</volume><pubmed_abstract>Krüppel-like factor 5 (KLF5) both suppresses and promotes tumor growth depending on cellular context. The mechanisms underlying tumor promotion could be targetable for therapy. Although a number of transcriptional targets of KLF5 have been identified and implicated in KLF5-mediated tumor growth, how KLF5 regulates these genes remains to be addressed. Here we performed coimmunoprecipitation (co-IP) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) in the TSU-Pr1 bladder cancer cell line, in which KLF5 is shown to promote tumor growth, to identify KLF5-interacting nuclear proteins that are necessary for KLF5's tumor promoting function. LC-MS/MS revealed 122 potential KLF5 binding proteins in the nuclear proteins precipitated by the KLF5 antibody, and the top nine candidates inclu</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>CINP is a novel cofactor of KLF5 required for its role in the promotion of cell proliferation, survival and tumor growth.</pubmed_title><pmcid>PMC6294659</pmcid><funding_grant_id>R01 CA171189</funding_grant_id><funding_grant_id>R01CA171189</funding_grant_id><funding_grant_id>81130044</funding_grant_id><pubmed_authors>Gao A</pubmed_authors><pubmed_authors>Qi L</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>An N</pubmed_authors><pubmed_authors>Liu M</pubmed_authors><pubmed_authors>Wu Q</pubmed_authors><pubmed_authors>Fu X</pubmed_authors><pubmed_authors>Dong JT</pubmed_authors><pubmed_authors>A J</pubmed_authors><pubmed_authors>Li M</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Fu C</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>King JL</pubmed_authors><pubmed_authors>Fu L</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Ci X</pubmed_authors><pubmed_authors>Ma G</pubmed_authors></additional><is_claimable>false</is_claimable><name>CINP is a novel cofactor of KLF5 required for its role in the promotion of cell proliferation, survival and tumor growth.</name><description>Krüppel-like factor 5 (KLF5) both suppresses and promotes tumor growth depending on cellular context. The mechanisms underlying tumor promotion could be targetable for therapy. Although a number of transcriptional targets of KLF5 have been identified and implicated in KLF5-mediated tumor growth, how KLF5 regulates these genes remains to be addressed. Here we performed coimmunoprecipitation (co-IP) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) in the TSU-Pr1 bladder cancer cell line, in which KLF5 is shown to promote tumor growth, to identify KLF5-interacting nuclear proteins that are necessary for KLF5's tumor promoting function. LC-MS/MS revealed 122 potential KLF5 binding proteins in the nuclear proteins precipitated by the KLF5 antibody, and the top nine candidates inclu</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Feb</publication><modification>2026-05-06T01:23:57.31Z</modification><creation>2020-10-29T11:01:41Z</creation></dates><accession>S-EPMC6294659</accession><cross_references><pubmed>30289973</pubmed><doi>10.1002/ijc.31908</doi></cross_references></HashMap>