FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000830882> ?p ?o ?g. }

• W2000830882 endingPage "3661" @default.
• W2000830882 startingPage "3651" @default.
• W2000830882 abstract "Metastasis of solid tumors is associated with poor prognosis and bleak survival rates. Tumor-infiltrating myeloid cells (TIMs) are known to promote metastasis, but the mechanisms underlying their collaboration with tumor cells remain unknown. Here, we report an oncogenic role for microRNA (miR) in driving M2 reprogramming in TIMs, characterized by the acquisition of pro-tumor and pro-angiogenic properties. The expression of miR-21, miR-29a, miR-142-3p and miR-223 increased in myeloid cells during tumor progression in mouse models of breast cancer and melanoma metastasis. Further, we show that these miRs are regulated by the CSF1-ETS2 pathway in macrophages. A loss-of-function approach utilizing selective depletion of the miR-processing enzyme Dicer in mature myeloid cells blocks angiogenesis and metastatic tumor growth. Ectopic expression of miR-21 and miR-29a promotes angiogenesis and tumor cell proliferation through the downregulation of anti-angiogenic genes such as Col4a2, Spry1 and Timp3, whereas knockdown of the miRs impedes these processes. miR-21 and miR-29a are expressed in Csf1r+ myeloid cells associated with human metastatic breast cancer, and levels of these miRs in CD115+ non-classical monocytes correlates with metastatic tumor burden in patients. Taken together, our results suggest that miR-21 and miR-29a are essential for the pro-tumor functions of myeloid cells and the CSF1-ETS2 pathway upstream of the miRs serves as an attractive therapeutic target for the inhibition of M2 remodeling of macrophages during malignancy. In addition, miR-21 and miR-29a in circulating myeloid cells may potentially serve as biomarkers to measure therapeutic efficacy of targeted therapies for CSF1 signaling." @default.
• W2000830882 created "2016-06-24" @default.
• W2000830882 creator A5013813215 @default.
• W2000830882 creator A5019267884 @default.
• W2000830882 creator A5021480812 @default.
• W2000830882 creator A5024627457 @default.
• W2000830882 creator A5025045936 @default.
• W2000830882 creator A5031622926 @default.
• W2000830882 creator A5040645408 @default.
• W2000830882 creator A5048499133 @default.
• W2000830882 creator A5051867478 @default.
• W2000830882 creator A5058858413 @default.
• W2000830882 creator A5073571156 @default.
• W2000830882 creator A5077991708 @default.
• W2000830882 creator A5084498101 @default.
• W2000830882 creator A5086903918 @default.
• W2000830882 date "2014-09-22" @default.
• W2000830882 modified "2023-10-18" @default.
• W2000830882 title "CSF1-ETS2-induced microRNA in myeloid cells promote metastatic tumor growth" @default.
• W2000830882 cites W1500151013 @default.
• W2000830882 cites W1536553403 @default.
• W2000830882 cites W1595293335 @default.
• W2000830882 cites W1648301895 @default.
• W2000830882 cites W1963904011 @default.
• W2000830882 cites W1965696083 @default.
• W2000830882 cites W1968138343 @default.
• W2000830882 cites W1970062316 @default.
• W2000830882 cites W1970264868 @default.
• W2000830882 cites W1980485314 @default.
• W2000830882 cites W1995386048 @default.
• W2000830882 cites W2005757388 @default.
• W2000830882 cites W2007196889 @default.
• W2000830882 cites W2008945738 @default.
• W2000830882 cites W2025041219 @default.
• W2000830882 cites W2031502153 @default.
• W2000830882 cites W2039183048 @default.
• W2000830882 cites W2048178760 @default.
• W2000830882 cites W2050444114 @default.
• W2000830882 cites W2057419005 @default.
• W2000830882 cites W2058648826 @default.
• W2000830882 cites W2059266855 @default.
• W2000830882 cites W2060672294 @default.
• W2000830882 cites W2067884710 @default.
• W2000830882 cites W2070855360 @default.
• W2000830882 cites W2072692158 @default.
• W2000830882 cites W2080037839 @default.
• W2000830882 cites W2090338505 @default.
• W2000830882 cites W2096573862 @default.
• W2000830882 cites W2100067750 @default.
• W2000830882 cites W2100218575 @default.
• W2000830882 cites W2103211592 @default.
• W2000830882 cites W2104669682 @default.
• W2000830882 cites W2104839914 @default.
• W2000830882 cites W2107277218 @default.
• W2000830882 cites W2110093634 @default.
• W2000830882 cites W2117776343 @default.
• W2000830882 cites W2118842534 @default.
• W2000830882 cites W2119985976 @default.
• W2000830882 cites W2120621109 @default.
• W2000830882 cites W2121936638 @default.
• W2000830882 cites W2122205306 @default.
• W2000830882 cites W2123509232 @default.
• W2000830882 cites W2125945390 @default.
• W2000830882 cites W2127079528 @default.
• W2000830882 cites W2127421703 @default.
• W2000830882 cites W2132485200 @default.
• W2000830882 cites W2137798077 @default.
• W2000830882 cites W2144370960 @default.
• W2000830882 cites W2153917851 @default.
• W2000830882 cites W2154674858 @default.
• W2000830882 cites W2155585495 @default.
• W2000830882 cites W2163035374 @default.
• W2000830882 cites W2163655902 @default.
• W2000830882 cites W2166859762 @default.
• W2000830882 cites W2167279371 @default.
• W2000830882 doi "https://doi.org/10.1038/onc.2014.294" @default.
• W2000830882 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4369473" @default.
• W2000830882 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25241894" @default.
• W2000830882 hasPublicationYear "2014" @default.
• W2000830882 type Work @default.
• W2000830882 sameAs 2000830882 @default.
• W2000830882 citedByCount "53" @default.
• W2000830882 countsByYear W20008308822015 @default.
• W2000830882 countsByYear W20008308822016 @default.
• W2000830882 countsByYear W20008308822017 @default.
• W2000830882 countsByYear W20008308822018 @default.
• W2000830882 countsByYear W20008308822019 @default.
• W2000830882 countsByYear W20008308822020 @default.
• W2000830882 countsByYear W20008308822021 @default.
• W2000830882 countsByYear W20008308822022 @default.
• W2000830882 crossrefType "journal-article" @default.
• W2000830882 hasAuthorship W2000830882A5013813215 @default.
• W2000830882 hasAuthorship W2000830882A5019267884 @default.
• W2000830882 hasAuthorship W2000830882A5021480812 @default.
• W2000830882 hasAuthorship W2000830882A5024627457 @default.
• W2000830882 hasAuthorship W2000830882A5025045936 @default.
• W2000830882 hasAuthorship W2000830882A5031622926 @default.
• W2000830882 hasAuthorship W2000830882A5040645408 @default.

• next