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NAC1 promotes stemness and regulates myeloid-derived cell status in triple-negative breast cancer.
Ngule, Chrispus; Shi, Ruyi; Ren, Xingcong; Jia, Hongyan; Oyelami, Felix; Li, Dong; Park, Younhee; Kim, Jinhwan; Hemati, Hami; Zhang, Yi; Xiong, Xiaofang; Shinkle, Andrew; Vanderford, Nathan L; Bachert, Sara; Zhou, Binhua P; Wang, Jianlong; Song, Jianxun; Liu, Xia; Yang, Jin-Ming.
Afiliación
  • Ngule C; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Shi R; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Ren X; Present Address: Department of Cell Biology and Genetics, Shanxi Medical University, Taiyuan, Shanxi, China.
  • Jia H; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Oyelami F; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Li D; Present Address: Department of Breast Surgery, First Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  • Park Y; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Kim J; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Hemati H; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Zhang Y; Department of Biochemistry, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Xiong X; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Shinkle A; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Vanderford NL; Present Address: Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, China.
  • Bachert S; Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, Bryan, TX, 77807, USA.
  • Zhou BP; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Wang J; Department of Toxicology and Cancer Biology, Department of Pharmacology and Nutritional Science, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Song J; Department of Pathology and Laboratory Medicine, University of Kentucky, Lexington, KY, 40536, USA.
  • Liu X; Department of Biochemistry, and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
  • Yang JM; Department of Medicine, Columbia Center for Human Development and Stem Cell Therapies, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Mol Cancer ; 23(1): 188, 2024 Sep 06.
Article en En | MEDLINE | ID: mdl-39243032
ABSTRACT
Triple negative breast cancer (TNBC) is a particularly lethal breast cancer (BC) subtype driven by cancer stem cells (CSCs) and an immunosuppressive microenvironment. Our study reveals that nucleus accumbens associated protein 1 (NAC1), a member of the BTB/POZ gene family, plays a crucial role in TNBC by maintaining tumor stemness and influencing myeloid-derived suppressor cells (MDSCs). High NAC1 expression correlates with worse TNBC prognosis. NAC1 knockdown reduced CSC markers and tumor cell proliferation, migration, and invasion. Additionally, NAC1 affects oncogenic pathways such as the CD44-JAK1-STAT3 axis and immunosuppressive signals (TGFß, IL-6). Intriguingly, the impact of NAC1 on tumor growth varies with the host immune status, showing diminished tumorigenicity in natural killer (NK) cell-competent mice but increased tumorigenicity in NK cell-deficient ones. This highlights the important role of the host immune system in TNBC progression. In addition, high NAC1 level in MDSCs also supports TNBC stemness. Together, this study implies NAC1 as a promising therapeutic target able to simultaneously eradicate CSCs and mitigate immune evasion.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Madre Neoplásicas / Proliferación Celular / Neoplasias de la Mama Triple Negativas / Células Supresoras de Origen Mieloide Límite: Animals / Female / Humans Idioma: En Revista: Mol Cancer Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Madre Neoplásicas / Proliferación Celular / Neoplasias de la Mama Triple Negativas / Células Supresoras de Origen Mieloide Límite: Animals / Female / Humans Idioma: En Revista: Mol Cancer Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido