bioRxiv Science⌕ Search

Biology subjects

Headley, M.

Publications and source records attributed to Headley, M..

2 recordsLinked to original sources

Apoptotic cells promote circulating tumor cell survival and metastasis

During tumor progression and especially following cytotoxic therapy, cell death of both tumor and stromal cells is widespread. Despite clinical observations that high levels of apoptotic cells correlate with poorer patient outcomes, the physiological effects of dying cells on tumor progression remain incompletely understood. Here, we report that circulating apoptotic cells robustly enhance tumor cell metastasis to the lungs. Using intravenous metastasis models, we observed that the presence of apoptotic cells, but not cells dying by other mechanisms, supports circulating tumor cell (CTC) survival following arrest in the lung vasculature. Apoptotic cells promote CTC survival by recruiting platelets to the forming metastatic niche. Apoptotic cells externalize the phospholipid phosphatidylserine to the outer leaflet of the plasma membrane, which we found increased the activity of the coagulation initiator Tissue Factor, thereby triggering the formation of platelet clots that protect proximal CTCs. Inhibiting the ability of apoptotic cells to induce coagulation by knocking out Tissue Factor, blocking phosphatidylserine, or administering the anticoagulant heparin abrogated the pro-metastatic effect of apoptotic cells. This work demonstrates a previously unappreciated role for apoptotic cells in facilitating metastasis by establishing CTC-supportive emboli, and suggests points of intervention that may reduce the pro-metastatic effect of apoptotic cells. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/595217v1_ufig1.gif" ALT="Figure 1"> View larger version (70K): org.highwire.dtl.DTLVardef@889460org.highwire.dtl.DTLVardef@c55e30org.highwire.dtl.DTLVardef@1aac38forg.highwire.dtl.DTLVardef@cf7ae_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Integrin αvβ8 on T cells is responsible for suppression of anti-tumor immunity in multiple syngeneic models and is a promising target for tumor immunotherapy

The v{beta}8 integrin is a key activator of transforming growth factor {beta} (TGF {beta}), which has been shown to inhibit anti-tumor immunity. Previous work has suggested that v{beta}8 on tumor cells could modulate tumor growth and responses to immune checkpoint blockade. We now show that a potent blocking monoclonal antibody against v{beta}8 (ADWA-11) causes growth suppression or complete regression in syngeneic models of squamous cell carcinoma (CCK168), mammary cancer (EMT-6), colon cancer (CT26), and prostate cancer (TRAMPC2), especially when it is combined with other immunomodulators (anti-PD-1, anti-CTLA-4 or 4-1BB) or radiotherapy. v{beta}8 is expressed on tumor cells in some of these models, but tumor cell expression of v{beta}8 is not essential for the beneficial effects of ADWA-11 therapy. v{beta}8 is consistently expressed at highest levels on CD4+CD25+ T cells within tumors, and specific deletion of Itgb8 from T cells is as effective as ADWA-11 in suppressing tumor growth. Treatment with ADWA-11 increases expression of a suite of genes in tumor infiltrating CD8+ T cells that are normally inhibited by TGF{beta} and are involved in tumor cell killing, including Granzyme B and Interferon-{gamma}. These findings solidify v{beta}8 integrin as a promising target for cancer immunotherapy, even for tumors that do not express this integrin.

cancer biology↗