biostudies-literatureLin Qthe Natural Science Foundation of ChinaProject of The Beijing Xisike Clinical Oncology Research FoundationClinical Innovation Project of Bioland Laboratorythe National Key R&D Program of Chinathe National Key R&D Program of ChinaKey Projects of The National Natural Science Foundation of ChinaProject of The Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene RegulationSun Yat-sen memorial hospital cultivation project for clinical researchTechnology Development Program of Guangdong provinceKey Projects of The National Natural Science Foundation of China5703https://www.ebi.ac.uk/biostudies/studies/S-EPMC8616231biostudies-literatureUnknown13(22)Bone metastasis from triple-negative breast cancer (TNBC) frequently results in poorer prognosis than other types of breast cancer due to the delay in diagnosis and intervention, lack of effective treatments and more skeletal-related complications. In the present study, we identified CTNND1 as a most reduced molecule in metastatic bone lesion from TNBC by way of high throughput sequencing of TNBC samples. In vivo experiments revealed that knockdown of CTNND1 enhanced tumor cells metastasis to bones and also increased neutrophils infiltration in bones. In vitro, we demonstrated that knockdown of CTNND1 accelerated epithelial-mesenchymal transformation (EMT) of tumor cells and their recruitment to bones. The involvement by CTNND1 in EMT and bone homing was achieved by upregulating CXCR4 via CancersSilencing CTNND1 Mediates Triple-Negative Breast Cancer Bone Metastasis via Upregulating CXCR4/CXCL12 Axis and Neutrophils Infiltration in Bone.PMC86162312021A0505030082SYS-C-2018052020B1212060018OF007(81672594 , 81772836 , 81872139 and 820729072018GZR02010042017YFC1309103 and 2017YFC130910451861125203Y-Roche2019/2-0078Fang XYang WLin QLuo QLi JGong CLiang GSanders AJJia SJiang WCen YShi YfalseSilencing CTNND1 Mediates Triple-Negative Breast Cancer Bone Metastasis via Upregulating CXCR4/CXCL12 Axis and Neutrophils Infiltration in Bone.Bone metastasis from triple-negative breast cancer (TNBC) frequently results in poorer prognosis than other types of breast cancer due to the delay in diagnosis and intervention, lack of effective treatments and more skeletal-related complications. In the present study, we identified CTNND1 as a most reduced molecule in metastatic bone lesion from TNBC by way of high throughput sequencing of TNBC samples. In vivo experiments revealed that knockdown of CTNND1 enhanced tumor cells metastasis to bones and also increased neutrophils infiltration in bones. In vitro, we demonstrated that knockdown of CTNND1 accelerated epithelial-mesenchymal transformation (EMT) of tumor cells and their recruitment to bones. The involvement by CTNND1 in EMT and bone homing was achieved by upregulating CXCR4 via 2021-01-01T00:00:00Z2021 Nov2026-06-19T03:08:20.293Z2026-06-19T03:07:03.106ZS-EPMC86162313483086210.3390/cancers13225703