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Macrophages expedite cell proliferation of prostate intraepithelial neoplasia through their downstream target ERK
Author(s) -
Thomas Mikalah U.,
Messex Justin K.,
Dang Tu,
Abdulkadir Sarki A.,
Jorcyk Cheryl L.,
Liou GeouYarh
Publication year - 2021
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.15541
Subject(s) - prostate cancer , inflammation , cancer research , prostate , ccl2 , macrophage , cell growth , mapk/erk pathway , cxcl1 , medicine , cancer , high grade prostatic intraepithelial neoplasia , immunology , intraepithelial neoplasia , biology , microbiology and biotechnology , signal transduction , chemokine , biochemistry , genetics , in vitro
Prostate cancer precursors, known as prostate intraepithelial neoplasia (PIN), require abnormal neoplastic cell proliferation to eventually develop into cancer cells. Our study indicated these precancerous lesions were able to recruit macrophages through expression of ICAM‐1 and CCR2. Once recruited, infiltrating macrophages secreted C5a, CXCL1, and CCL2 all of which activated ERK signaling in PIN cells to expedite cell proliferation of PIN.