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http://purl.uniprot.org/citations/36627608http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36627608http://www.w3.org/2000/01/rdf-schema#comment"Human epidermal growth factor receptor 2-positive (HER2+) breast cancer is characterized by invasive growth, rapid metastasis and chemoresistance. Trastuzumab is an effective treatment for HER2+ breast cancer; however, trastuzumab resistance leads to cancer relapse and metastasis. CKLF-like MARVEL transmembrane domain-containing 6 (CMTM6) has been considered as a new immune checkpoint for tumor-induced immunosuppression. The role of CMTM6 in trastuzumab resistance remains unknown. Here, we uncover a role of CMTM6 in trastuzumab-resistant HER2+ breast cancer. CMTM6 expression was upregulated in trastuzumab-resistant HER2+ breast cancer cell. Patients with high CMTM6 expressing HER2+ breast cancer had worse overall and progression-free survival than those with low CMTM6 expression. In vitro, CMTM6 knockdown inhibited the proliferation and migration of HER2+ breast cancer cells, and promoted their apoptosis, while CMTM6 overexpression reversed these effects. CMTM6 and HER2 proteins were co-localized on the surface of breast cancer cells, and CMTM6 silencing reduced HER2 protein levels in breast cancer cells. Co-immunoprecipitation revealed that CMTM6 directly interacted with HER2 in HER2+ breast cancer cells, and CMTM6 overexpression inhibited HER2 ubiquitination. Collectively, these findings highlight that CMTM6 stabilizes HER2 protein, contributing to trastuzumab resistance and implicate CMTM6 as a potential prognostic marker and therapeutic target for overcoming trastuzumab resistance in HER2+ breast cancer."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.org/dc/terms/identifier"doi:10.1186/s12943-023-01716-y"xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Gao H."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Liu C."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Sun J."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Sun L."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Xue J."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Qiao X."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/author"Xing F."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/name"Mol Cancer"xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/pages"6"xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/title"CMTM6 overexpression confers trastuzumab resistance in HER2-positive breast cancer."xsd:string
http://purl.uniprot.org/citations/36627608http://purl.uniprot.org/core/volume"22"xsd:string
http://purl.uniprot.org/citations/36627608http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/36627608
http://purl.uniprot.org/citations/36627608http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/36627608
http://purl.uniprot.org/uniprot/#_Q9NX76-mappedCitation-36627608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36627608
http://purl.uniprot.org/uniprot/#_Q9P1E2-mappedCitation-36627608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36627608
http://purl.uniprot.org/uniprot/Q9NX76http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36627608
http://purl.uniprot.org/uniprot/Q9P1E2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36627608