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. 2023 Mar 14;8:116. doi: 10.1038/s41392-023-01343-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — The mechanisms for cellular reprogramming in cancer. Cancer cell reprogramming treatment aims to convert the malignancy to benignity or provide a therapeutic target to inhibit the formation of CSCs. Yamanaka factors-mediated iPSCs technology has been recognized as a common method for the conversion of cancer cells to benign pluripotent cells, and cancer cells-derived iPSCs can re-differentiate into functional cells with less malignancy and free of tumorigenic potential. Cancer cells also can be directly reprogrammed into benign cells via various reprogramming strategies, such as lineage-specific factors, small molecules, microRNAs, and exosomes. Responsive cellular reprogramming based on EMT contributes to CSCs formation, which mediates the initial, progression, metastasis, and post-treatment recurrence. The role of cellular reprogramming in the formation of CSCs suggests that anti-cellular reprogramming strategies may be considered as a therapeutic alternative in cancer treatment. EMT Epithelial–mesenchymal transition. Created with BioRender.com