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J Immunol Res ; 2024: 3145695, 2024.
Article in English | MEDLINE | ID: mdl-38983273

ABSTRACT

Background: This work focused on investigating the role of programmed death ligand 2 (PD-L2) in the progression of breast cancer by utilizing breast cancer specimens and cells. Materials and Methods: The serum levels of soluble PD-L2 (sPD-L2) in breast cancer patients and healthy individuals were analyzed by means of the enzyme-linked immunosorbent assay, and the PD-L2 levels within 416 resected breast cancer specimens were assessed through immunohistochemistry. Concurrently, in vitro cell experiments and in vivo animal experiments were carried out to analyze the relationship between PD-L2 and the invasion and migration of breast cancer. Results: The concentration of sPD-L2 in breast cancer patients significantly increased compared to that in the control groups. Additionally, breast cancer patients with high concentrations of sPD-L2 had higher Ki67 values (≥30%) and tumor grades. PD-L2 was expressed in 79.09% of the cancer samples, which exhibited a positive correlation with the progesterone receptor (PR) and the human epidermal growth factor receptor 2 (HER2). Furthermore, we discovered that knockdown of PD-L2 inhibited the migratory and invasive abilities of both MCF-7 and MDA-MB231 cells. Conclusion: Our findings demonstrated that knockdown of PD-L2 suppressed tumor growth, providing novel insights into important biological functions.


Subject(s)
Breast Neoplasms , Cell Movement , Disease Progression , Programmed Cell Death 1 Ligand 2 Protein , Humans , Female , Breast Neoplasms/pathology , Breast Neoplasms/metabolism , Breast Neoplasms/genetics , Animals , Programmed Cell Death 1 Ligand 2 Protein/metabolism , Programmed Cell Death 1 Ligand 2 Protein/genetics , Mice , Cell Line, Tumor , Middle Aged , Receptor, ErbB-2/metabolism , Receptor, ErbB-2/genetics , Adult , Cell Proliferation , MCF-7 Cells , Gene Expression Regulation, Neoplastic , Neoplasm Invasiveness , Aged , Immunohistochemistry , Neoplasm Grading , Biomarkers, Tumor/metabolism , Disease Models, Animal , Receptors, Progesterone/metabolism , Gene Knockdown Techniques
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