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- Title
Bleomycin inhibits proliferation and induces apoptosis in TPC‑1 cells through reversing M2‑macrophages polarization.
- Authors
Liu, Hongwei; Dong, Huilei; Jiang, Li; Li, ZhENdong; Ma, Xiande
- Abstract
Papillary thyroid carcinoma (PTC) is one of the most common types of thyroid malignancy. Previous studies have demonstrated that the density of tumor‑associated macrophages (TAMs) within the tumor microenvironment affects the progression of PTC due to the imbalance in M1/M2 macrophage subtypes. M2 macrophages induce anti‑inflammatory effects and promote tumor progression, whereas M1 macrophages destroy tumor cells. Therefore, reversing TAM polarization to M1 may be a novel strategy for the treatment of cancer. Although bleomycin (BLM) is a commonly used anti‑cancer drug, which regulates the secretion of relevant cytokines, high dose and long‑term treatment with BLM may lead to pulmonary fibrosis. In the present study, flow cytometry data revealed that low dose treatment with BLM (5 or 10 mU/ml) facilitated the expression of the M1 phenotype markers cluster of differentiation (CD)80 and C‑C chemokine receptor 7, and concurrently suppressed the M2 marker CD206 on M2‑macrophages. Reverse transcription‑quantitative polymerase chain reaction data revealed that the expression levels of tumor necrosis factor‑α and interleukin‑1β markedly increased, whereas the expression of IL‑10 decreased in M2 macrophages treated with BLM. A fluorescein isothiocyanate‑dextran uptake experiment revealed that BLM increased the phagocytic capacity of M2, however not M1 or M0 macrophages. In addition, to verify the effect of BLM‑treated M2 macrophages on thyroid carcinoma cells, a co‑culture system of macrophages and the human PTC cell line TPC‑1, was established. BLM‑treated M2 macrophages increased the number of cells in early and late apoptosis and inhibited the migration, proliferation and invasion of TPC‑1 cells. These results suggest that a low dose and indirect effect of BLM may induce suppressive effects on PTC by selectively reversing M2 macrophage polarization to M1, which may provide a novel strategy for cancer treatment.
- Subjects
THYROID cancer; PAPILLARY carcinoma; CANCER immunology; BLEOMYCIN; CANCER cell proliferation; MACROPHAGES; THERAPEUTICS
- Publication
Oncology Letters, 2018, Vol 16, Issue 3, p3858
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2018.9103