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Time-Lapse 2D Imaging of Phagocytic Activity in M1 Macrophage-4T1 Mouse Mammary Carcinoma Cells in Co-cultures
Published on: December 14, 2019
miR-34c-3p Inhibits Nasopharyngeal Carcinoma Development via Inhibiting M2 Polarization of Macrophages
Yu Zi Ji1, Yu Jie Wang1, Ji Qing Ma1
1Department of Otolaryngology Head and Neck surgery, Henan Provincial People's Hospital (People's Hospital of Zhengzhou University), Zhengzhou 450003, Henan, China.
Objective:
miR-34c-3p is down-regulated in nasopharyngeal carcinoma (NPC). The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.
Methods:
Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86 (CD86) and cluster of differentiation 206 (CD206) expression; quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were employed to examine mRNA expression and protein levels; cell counting kit-8 (CCK8) and transwell assays were employed to assess cell proliferation, migration, and invasion; and hematoxylin-eosin (HE) staining was employed to assess pathological changes in tumor tissues.
Results:
Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11, and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation, migration, and invasion of NPC cells. The in vivo experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.
Conclusion:
This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.
Insights
MicroRNA 34c-3p (miR-34c-3p) inhibits nasopharyngeal carcinoma (NPC) progression by targeting SLC7A11 and suppressing M2 macrophage polarization. This finding offers a potential new therapeutic strategy for NPC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Nasopharyngeal carcinoma (NPC) is a prevalent head and neck cancer.
- The role and mechanism of miR-34c-3p in NPC remain largely unexplored.
- Down-regulation of miR-34c-3p is observed in NPC tissues.
Purpose of the Study:
- To investigate the biological function of miR-34c-3p in NPC.
- To elucidate the underlying molecular mechanisms of miR-34c-3p action in NPC.
- To evaluate miR-34c-3p as a potential therapeutic target for NPC.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to assess miR-34c-3p, CD86, and CD206 expression.
- Cell counting kit-8 (CCK8) and transwell assays were performed to evaluate NPC cell proliferation, migration, and invasion.
- Flow cytometry, immunohistochemistry, and hematoxylin-eosin (HE) staining were utilized to analyze macrophage polarization and tumor pathology.
Main Results:
- miR-34c-3p mimic transfection inhibited M2 macrophage polarization by targeting SLC7A11.
- M2 macrophages transfected with miR-34c-3p mimic suppressed NPC cell proliferation, migration, and invasion.
- In vivo studies demonstrated that miR-34c-3p mimics inhibited tumor growth and reduced inflammatory infiltration.
Conclusions:
- miR-34c-3p plays a crucial role in regulating NPC progression.
- Targeting miR-34c-3p offers a novel therapeutic strategy for NPC.
- This study provides new insights into NPC pathogenesis and treatment.
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