The related mechanism by which p16 regulates the tumor immune microenvironment. (IMAGE)
Caption
(A) In Kras-driven lung cancer, senescent alveolar macrophages and endothelial cells accumulate early in the tumor, but only macrophages display a unique signature of secreted SASP factors. Ablation of p16INK4a-expressing cells in tumor-bearing mice treated with DT or ABT-737 significantly increased the proportion of CD4+ and CD8+ T lymphocytes in the TME, reduced the number of Tregs, abolished normal tumor angiogenesis, and inhibited tumor growth. (B) In Kras-driven lung cancer, senescent alveolar macrophages accumulate early in the tumor, showing increased p16INK4a and CXCR1 expression, and they inhibit CTL responses. Removing these macrophages or knocking out the p16 gene reduces CXCR1 levels, leading to increased CTL accumulation in the microenvironment and the inhibition of tumor progression.
Credit
Qingbo Zhu, Xiaoli Wei, Ziting Qu, Lili Lu, Yiyin Zhang, Hua Wang
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