Publications by authors named "M Ducka"

The transcription factor c-Myb is an oncoprotein promoting cell proliferation and survival when aberrantly activated/expressed, thus contributing to malignant transformation. Overexpression of c-Myb has been found in leukemias, breast, colon and adenoid cystic carcinoma. Recent studies revealed its expression also in osteosarcoma cell lines and suggested its functional importance during bone development.

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The transcription factor c-Myb can be involved in the activation of many genes with protumorigenic function; however, its role in breast cancer (BC) development is still under discussion. c-Myb is considered as a tumor-promoting factor in the early phases of BC, on the other hand, its expression in BC patients relates to a good prognosis. Previously, we have shown that c-Myb controls the capacity of BC cells to form spontaneous lung metastasis.

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Tumor-associated macrophages (TAMs) are prominent components of tumor stroma that promotes tumorigenesis. Many soluble factors participate in the deleterious cross-talk between TAMs and transformed cells; however mechanisms how tumors orchestrate their production remain relatively unexplored. c-Myb is a transcription factor recently described as a negative regulator of a specific immune signature involved in breast cancer (BC) metastasis.

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Wedelactone (WL), a plant polyphenolic derivative of coumestan, represents a promising anti-cancer agent. The underlying mechanisms of its action are not fully understood and appear to involve interplay with copper ions. Herein, we examined coordination and redox interactions of WL with Cu in phosphate buffer (pH 7), and in two breast cancer cell lines.

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Article Synopsis
  • Metastasis is a major cause of cancer-related deaths, with specific interactions between tumor cells and their surrounding environment playing a critical role in this process.
  • The transcription factor c-Myb is linked to breast cancer progression; however, this study reveals that higher c-Myb levels actually inhibit lung metastasis by disrupting the ability of tumor cells to exit blood vessels.
  • Cells with lower c-Myb levels show increased metastatic potential and are associated with an inflammatory signature dominated by Ccl2, indicating that c-Myb may help reduce inflammation and prevent lung metastasis in breast cancer patients.
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