지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2025.3
- 수록면
- 37 - 48 (12page)
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초록· 키워드
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Importance: Chemokines and their receptors play integral roles in carcinogenesis. CXC motif chemokine receptor 3 (CXCR3) in T cells mediates anti-tumor effects, whereas CXCR3 in malignant cells promotes proliferation and metastasis. Although the role of CXCR3 has been well-documented in human cancers, including breast cancer, its function in canine tumors remains largely unexplored.
Objective: This study aimed to investigate the effects of CXCR3 and its ligand interaction in canine mammary gland tumor (cMGT) cells.
Methods: CXCR3 expression in two cMGT cell lines, CIPp and CIPm, was evaluated using real-time quantitative polymerase chain reaction, western blotting, and flow cytometry. CXC motif chemokine ligand 10 (CXCL10)-induced changes in CXCR3 protein expression in cMGT cells were assessed using membrane fractionation assays. Cell proliferation and migration in response to CXCL10 treatment were analyzed using Cell Counting Kit-8 and wound-healing assays, respectively. Additionally, the downstream molecular mechanisms of the CXCL10/CXCR3 axis were examined.
Results: CXCR3 expression was significantly higher in CIPm than in CIPp cells. In both the cMGT cell lines, CXCL10 treatment reduced CXCR3 expression on the cell membrane in a dose- and time-dependent manner. The CXCR10/CXCR3 axis promoted cell proliferation and migration in cMGT cells. CXCL10/CXCR3 interaction upregulated the phosphorylation of AKT1 and ERK.
Conclusions and Relevance: This study demonstrates that the CXCL10/CXCR3 axis may contribute to the pathogenesis of cMGTs by promoting tumor cell proliferation and migration. CXCR3 signaling represents a potential therapeutic target for cMGTs.
Objective: This study aimed to investigate the effects of CXCR3 and its ligand interaction in canine mammary gland tumor (cMGT) cells.
Methods: CXCR3 expression in two cMGT cell lines, CIPp and CIPm, was evaluated using real-time quantitative polymerase chain reaction, western blotting, and flow cytometry. CXC motif chemokine ligand 10 (CXCL10)-induced changes in CXCR3 protein expression in cMGT cells were assessed using membrane fractionation assays. Cell proliferation and migration in response to CXCL10 treatment were analyzed using Cell Counting Kit-8 and wound-healing assays, respectively. Additionally, the downstream molecular mechanisms of the CXCL10/CXCR3 axis were examined.
Results: CXCR3 expression was significantly higher in CIPm than in CIPp cells. In both the cMGT cell lines, CXCL10 treatment reduced CXCR3 expression on the cell membrane in a dose- and time-dependent manner. The CXCR10/CXCR3 axis promoted cell proliferation and migration in cMGT cells. CXCL10/CXCR3 interaction upregulated the phosphorylation of AKT1 and ERK.
Conclusions and Relevance: This study demonstrates that the CXCL10/CXCR3 axis may contribute to the pathogenesis of cMGTs by promoting tumor cell proliferation and migration. CXCR3 signaling represents a potential therapeutic target for cMGTs.
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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