<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Deng B</submitter><funding>National Natural Science Foundation of China</funding><pagination>237</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11227718</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(1)</volume><pubmed_abstract>Coiled-coil domain containing 88C (CCDC88C) is a component of non-canonical Wnt signaling, and its dysregulation causes colorectal cancer metastasis. Dysregulated expression of CCDC88C was observed in lymph node metastatic tumor tissues of breast cancer. However, the role of CCDC88C in breast cancer metastasis remains unclear. To address this, the stable BT549 and SKBR3 cell lines with CCDC88C overexpression or knockdown were developed. Loss/gain-of-function experiments suggested that CCDC88C drove breast cancer cell motility in vitro and lung and liver metastasis in vivo. We found that CCDC88C led to c-JUN-induced transcription activation. Overlapping genes were identified from the genes modulated by CCDC88C and c-JUN. CEMIP, one of these overlapping genes, has been confirmed to confer br</pubmed_abstract><journal>Cancer cell international</journal><pubmed_title>CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription.</pubmed_title><pmcid>PMC11227718</pmcid><funding_grant_id>82103491</funding_grant_id><pubmed_authors>Deng B</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Sun T</pubmed_authors><pubmed_authors>Miao Y</pubmed_authors><pubmed_authors>Li A</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Fei J</pubmed_authors></additional><is_claimable>false</is_claimable><name>CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription.</name><description>Coiled-coil domain containing 88C (CCDC88C) is a component of non-canonical Wnt signaling, and its dysregulation causes colorectal cancer metastasis. Dysregulated expression of CCDC88C was observed in lymph node metastatic tumor tissues of breast cancer. However, the role of CCDC88C in breast cancer metastasis remains unclear. To address this, the stable BT549 and SKBR3 cell lines with CCDC88C overexpression or knockdown were developed. Loss/gain-of-function experiments suggested that CCDC88C drove breast cancer cell motility in vitro and lung and liver metastasis in vivo. We found that CCDC88C led to c-JUN-induced transcription activation. Overlapping genes were identified from the genes modulated by CCDC88C and c-JUN. CEMIP, one of these overlapping genes, has been confirmed to confer br</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2025-04-26T05:36:44.617Z</modification><creation>2025-04-06T11:37:33.014Z</creation></dates><accession>S-EPMC11227718</accession><cross_references><pubmed>38971758</pubmed><doi>10.1186/s12935-024-03413-2</doi></cross_references></HashMap>