Type 1 conventional dendritic cells (cDC1s) are key antigen-presenting cells (APCs) for cross-priming of CD8+ T cells against cancer. They can capture and cross-present dead cell antigens via DNGR-1 (CLEC9A), a receptor for F-actin exposed on cell corpses. However, cDC1s are scarce in human and murine tumors, and this restricts anticancer immunity. We show that abundant tumor-associated APCs, including cDC2s and monocyte-derived cells, can be redirected to internalize necrotic debris and cross-present associated antigens by a variety of reagents that bridge F-actin to Fcγ receptors (FcγRs), including an Fc-DNGR-1 fusion protein and an anti-F-actin antibody. In vivo, Fc-DNGR-1 accumulates in necrotic tumor areas and highlights their proximity to intratumoral FcγR+ APCs. In mouse cancer models, F-actin-FcγR bridging enhances tumor control and synergizes with cytotoxic chemotherapy or radiotherapy. Thus, nonspecialized APCs can be harnessed for cross-presentation of necrotic tumor antigens, and F-actin-FcγR bridging constitutes a strategy to potentiate anticancer immunity.