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. 2021 Jul 21;12:714822. doi: 10.3389/fimmu.2021.714822

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Copyright © 2021 Zimmermannova, Caiado, Ferreira and Pereira

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Disrupting cancer cell tumorigenicity with cellular reprogramming. Several tumor cell types have been described to be amenable to cell reprogramming towards induced pluripotent stem cells (iPSCs). Melanoma, glioblastoma, sarcoma, gastrointestinal (GI), as well as breast, bladder, and liver cancers, acute myeloid leukemia (AML), and chronic myelogenous leukemia (CML) have all been successfully reprogrammed towards iPSC with OCT4, SOX2, KLF4, and c-MYC. Following reprogramming to iPSCs, cancer cells can be differentiated into benignity by either differentiation to their original cell type or by converting them into a different lineage (highlighted by the colored lines). Similarly, in vitro direct reprogramming has been demonstrated in glioma, B-cell acute leukemia (B-ALL), Burkitt lymphoma (BL), squamous cell carcinoma (SCC), and hepatic cellular carcinoma (HCC). Lineage-specific factors rewrite the cancerous epigenetic and transcriptional program into mature terminally differentiated cells (glioma to neuron; SCC to melanocyte; HCC to hepatocyte), or by modifying cell fate and therefore disrupting the tumorigenic drive [B-leukemias to macrophage (MØ)].