<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ansems M</submitter><funding>KWF Kankerbestrijding</funding><pagination>693-703</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4326655</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>149(3)</volume><pubmed_abstract>Breast cancer is one of the most common causes of cancer-related deaths in women. The estrogen receptor (ERα) is well known for having growth promoting effects in breast cancer. Recently, we have identified DC-SCRIPT (ZNF366) as a co-suppressor of ERα and as a strong and independent prognostic marker in ESR1 (ERα gene)-positive breast cancer patients. In this study, we further investigated the molecular mechanism on how DC-SCRIPT inhibits breast cancer cell growth. DC-SCRIPT mRNA levels from 190 primary ESR1-positive breast tumors were related to global gene expression, followed by gene ontology and pathway analysis. The effect of DC-SCRIPT on breast cancer cell growth and cell cycle arrest was investigated using novel DC-SCRIPT-inducible MCF7 breast cancer cell lines. Genome-wide expressi</pubmed_abstract><journal>Breast cancer research and treatment</journal><pubmed_title>DC-SCRIPT is a novel regulator of the tumor suppressor gene CDKN2B and induces cell cycle arrest in ERα-positive breast cancer cells.</pubmed_title><pmcid>PMC4326655</pmcid><funding_grant_id>KUN 2011-5229</funding_grant_id><pubmed_authors>Smid M</pubmed_authors><pubmed_authors>de Weerd V</pubmed_authors><pubmed_authors>Foekens JA</pubmed_authors><pubmed_authors>de Graaf AM</pubmed_authors><pubmed_authors>Zuidscherwoude M</pubmed_authors><pubmed_authors>Martens JW</pubmed_authors><pubmed_authors>Sieuwerts AM</pubmed_authors><pubmed_authors>Ansems M</pubmed_authors><pubmed_authors>Sondergaard JN</pubmed_authors><pubmed_authors>Looman MW</pubmed_authors><pubmed_authors>Adema GJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>DC-SCRIPT is a novel regulator of the tumor suppressor gene CDKN2B and induces cell cycle arrest in ERα-positive breast cancer cells.</name><description>Breast cancer is one of the most common causes of cancer-related deaths in women. The estrogen receptor (ERα) is well known for having growth promoting effects in breast cancer. Recently, we have identified DC-SCRIPT (ZNF366) as a co-suppressor of ERα and as a strong and independent prognostic marker in ESR1 (ERα gene)-positive breast cancer patients. In this study, we further investigated the molecular mechanism on how DC-SCRIPT inhibits breast cancer cell growth. DC-SCRIPT mRNA levels from 190 primary ESR1-positive breast tumors were related to global gene expression, followed by gene ontology and pathway analysis. The effect of DC-SCRIPT on breast cancer cell growth and cell cycle arrest was investigated using novel DC-SCRIPT-inducible MCF7 breast cancer cell lines. Genome-wide expressi</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Feb</publication><modification>2026-04-13T08:48:51.349Z</modification><creation>2019-03-27T01:45:09Z</creation></dates><accession>S-EPMC4326655</accession><cross_references><pubmed>25663546</pubmed><doi>10.1007/s10549-015-3281-y</doi></cross_references></HashMap>