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Abstract
BackgroundThe antibiotic minocycline has been suggested as a potential agent in cancer therapy due to its anti-inflammatory properties and effectiveness as an NF-κB inhibitor. In previous studies, we showed that minocycline could effectively block the fusion of breast epithelial cells and cancer cells. However, its influence on breast cancer cell characteristics, including proliferation, migration, and gene expression has not yet been investigated.MethodsM13SV1-EGFP-Neo breast epithelial cells, HS578T-Hyg breast cancer cells and M13HS-2 and M13HS-8 tumor hybrids were used as breast (cancer) model cell lines in this study. Cells were treated with up to 50 µg/ml minocycline. An XTT assay and a colony formation assay were used to study cell proliferation. Western blot analysis and Zymography were used to examine the expression of MMP-2 and MMP-9, EMT, and stemness marker. Cell migration was measured by Scratch assay. Using a two-way ANOVA and the Tukey post-hoc test, statistical significance was determined.ResultsMinocycline inhibited proliferation and colony formation capacity in a dose-dependent manner, whereas EMT and stemness marker expression remained unchanged in all cell lines. Zymography data showed that MMP-2 and MMP-9 expression was down-regulated M13SV1-EGFP-Neo treated with minocycline, but not in HS578T-Hyg cells or M13HS-2 and M13HS-8 tumor hybrids. Minocycline inhibited the migration of M13SV1-EGFP-Neo cells in a dose-dependent manner, while the migration of HS578T-Hyg, M13HS-2 and M13HS-8 tumor hybrid cells necessitated a minimum of 25 µg/ml minocycline,ConclusionsThe results showed that non-malignant cells and neoplastic cells reacted differently to minocycline. This could mean that minocycline will have unwanted side effects if it is used in cancer therapy.
Highlights
Minocycline is a well-known second-generation tetracycline derivative [1, 2]
Minocycline significantly reduced cell proliferation in a dose dependent manner First, the proliferation of M13SV1-enhanced green fluorescent protein (EGFP)-Neo, HS578THyg, M13HS-2 and M13HS−8 cells was examined in relation to different concentrations of minocycline (0 μg/ml, 5 μg/ml, 10 μg/ml, 25 μg/ml, and 50 μg/ml)
A weak, but still detectable cell proliferation was observed for all cell lines in the presence of 10 μg/ml minocycline (Fig. 1a-d)
Summary
Minocycline is a well-known second-generation tetracycline derivative [1, 2]. Apart from its widespread application as an antibiotic, minocycline possesses anti-inflammatory, neuroprotective, and even anti-tumorigenic characteristics. Yang et al found that minocycline directly binds the Src kinase Lyn, thereby inactivating signal transducer and activator of transcription 3 (STAT3) signaling concomitant with suppression of epithelial-to-mesenchymal transition (EMT) and colorectal cancer metastasis [8] These results suggest that minocycline interferes with the transcription machinery in (cancer) cells. Minocycline inhibited the migration of M13SV1-EGFP-Neo cells in a dose-dependent manner, while the migration of HS578T-Hyg, M13HS-2 and M13HS-8 tumor hybrid cells necessitated a minimum of 25 μg/ml minocycline, Conclusions The results showed that non-malignant cells and neoplastic cells reacted differently to minocycline. This could mean that minocycline will have unwanted side effects if it is used in cancer therapy
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