AI Article Synopsis
- The inflammatory tumor microenvironment (TME) significantly contributes to cancer progression, particularly in prostate cancer.
- Tumor-associated macrophages (especially M1, pro-inflammatory types) promote cancer stemness while suppressing androgen response in prostate cancer cells.
- The study suggests that M1 macrophages do this by releasing factors that activate the NFκB signaling pathway, leading to increased expression of cancer stem cell markers like NANOG and KLF4.
Article Abstract
The inflammatory tumor microenvironment (TME) is a key driver for tumor-promoting processes. Tumor-associated macrophages are one of the main immune cell types in the TME and their increased density is related to poor prognosis in prostate cancer. Here, we investigated the influence of pro-inflammatory (M1) and immunosuppressive (M2) macrophages on prostate cancer lineage plasticity. Our findings reveal that M1 macrophage secreted factors upregulate genes related to stemness while downregulating genes associated with androgen response in prostate cancer cells. The expression of cancer stem cell (CSC) plasticity markers NANOG, KLF4, , and CD44 was stimulated by the secreted factors from M1 macrophages. Moreover, AR and its target gene were observed to be suppressed in LNCaP cells treated with secreted factors from M1 macrophages. Inhibition of NFκB signaling using the IKK16 inhibitor resulted in downregulation of NANOG, , and and CSC plasticity. Our study highlights that the secreted factors from M1 macrophages drive prostate cancer cell plasticity by upregulating the expression of CSC plasticity markers through NFκB signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11340773 | PMC |
| http://dx.doi.org/10.1080/2162402X.2024.2393442 | DOI Listing |
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