KLF-7 promotes progression of HNSCC by enhancing macrophage recruitment through LOX-mediated extracellular matrix remodeling.
KLF-7 acts as an oncogenic transcription factor in HNSCC by activating LOX to remodel the extracellular matrix and recruit tumor-associated macrophages.
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Aberrantly high activation of oncogenic transcription factors has been implicated in initiation and progression of malignant diseases. However, the landscape of dysregulated TFs in HNSCC remains poorly characterized, and especially their biological contributions to remodeling of cancer immune microenvironment are unknown. Here, by globally investigating oncogenic TF-target interactions in clinic, we identified that KLF-7 is one of the most potential oncogenic TFs in HNSCC. In vitro and in vivo experiments showed that KLF-7 governs not only the autonomous malignant behaviors but also recruitment of macrophage in the cancer microenvironment, consequently promoting progression of HNSCC in a tumor-associated macrophage (TAM) dependent manner. Mechanistically, we found that LOX is a bona fide target directly transcriptionally activated by KLF-7 in HNSCC cells. In vivo assay showed that LOX-driven crosslinking of extracellular matrix conducted a stiff extracellular matrix environment for macrophage recruitment and consequent disruption of CD8
Fan et al. (Wed,) reported a other. KLF-7 promotes progression of HNSCC by enhancing macrophage recruitment through LOX-mediated extracellular matrix remodeling.
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