Related Experiment Video
Updated: Feb 20, 2026

Novel Protocol for Generating Physiologic Immunogenic Dendritic Cells
Published on: May 17, 2019
miR-128 enhances dendritic cell-mediated anti-tumor immunity via targeting of p38
Xue Liang1, Wenfeng Shangguan1, Miaomiao Zhang2
1Department of Cardiology, Tianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Abstract:
MiRNA (miR)-128, which is a well‑recognized inhibitor of tumor growth, is involved in the anti-tumor function of dendritic cells (DCs). However, the association between miR‑128 and the DC‑mediated anti‑tumor immunity remains to be elucidated. Murine B16 melanoma cells and C57BL/6 male mice were used to obtain marrow‑derived DCs. DCs were treated with B16 cell suspension. miR‑128 mimic, miR‑128 inhibitor, p38 inhibitor or negative control oligonucleotides were transfected into DCs. After transfection, mRNA and protein expression of p38 in DCs was detected via reverse transcription‑quantitative polymerase chain reaction and western blotting. The present study demonstrated that the miR‑128 abundance in DCs was significantly attenuated by B16 (a melanoma cell line) stimulation and the protein expression level of p38 was increased. Additionally, miR‑128 inhibited the protein expression of p38 in DCs in a dose‑dependent manner, however no significant effect on the p38 mRNA level was observed. Furthermore, miR‑128 mimic or p38 inhibitor decreased the mRNA expression and secretion of interleukin (IL)‑6 and IL‑10 cytokines and increased the level of IL‑12 in DCs, whereas an miR‑128 inhibitor exhibited the opposite effects. These findings suggested that miR‑128 regulated the immune response of DCs via p38‑downstream cytokines. Furthermore, the tumor growth rate, size and weight were markedly decreased and the survival time prolonged, following injection of DCs harboring miR‑128 mimic or p38 inhibitor in C57BL/6 mice bearing B16 melanoma. The results therefore suggest that miR‑128 enhances the anti‑tumor immunity response of DCs via targeting of the p38 mitogen activated protein kinase signaling pathway.
Insights
MicroRNA (miR)-128 enhances anti-tumor immunity by dendritic cells (DCs) through the p38 signaling pathway. This study shows miR-128 targets p38, modulating cytokine secretion and inhibiting melanoma tumor growth.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- MicroRNA (miR)-128 is a known tumor growth inhibitor.
- Dendritic cells (DCs) play a crucial role in anti-tumor immunity.
- The specific role of miR-128 in DC-mediated anti-tumor immunity requires further investigation.
Purpose of the Study:
- To elucidate the association between miR-128 and DC-mediated anti-tumor immunity.
- To investigate the mechanism by which miR-128 influences DC function.
- To evaluate the therapeutic potential of modulating miR-128 in a melanoma model.
Main Methods:
- Murine B16 melanoma cells and C57BL/6 mice were used.
- Dendritic cells (DCs) were derived and stimulated with B16 cells.
- miR-128 mimic/inhibitor and p38 inhibitor were transfected into DCs.
- mRNA and protein expression of p38, and cytokine levels (IL-6, IL-10, IL-12) were analyzed.
- Tumor growth and survival were assessed in a B16 melanoma mouse model.
Main Results:
- B16 melanoma stimulation reduced miR-128 abundance and increased p38 protein expression in DCs.
- miR-128 inhibited p38 protein expression in a dose-dependent manner, without affecting mRNA levels.
- Modulation of miR-128 or p38 affected the secretion of IL-6, IL-10, and IL-12.
- DCs engineered with miR-128 mimic or p38 inhibitor significantly reduced tumor growth and prolonged survival in mice.
Conclusions:
- miR-128 regulates DC immune response via p38-downstream cytokines.
- miR-128 enhances anti-tumor immunity of DCs by targeting the p38 mitogen-activated protein kinase signaling pathway.
- Modulating miR-128 in DCs represents a potential strategy for melanoma immunotherapy.
Related Concept Videos
Abnormal Proliferation
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

