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. 2023 Mar 22;42:69. doi: 10.1186/s13046-023-02641-0

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© The Author(s) 2023

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Workflow of the multi-omics integrative analysis. Biological System: H460 LUAD and MCF7 breast cancer cell lines were cultured in 2D and 3D conditions. 3D tumor spheroids were grown either in a nutrient-rich (sphere medium, SM) or in a nutrient-restricted (FBS^low) culture media. Input: a total of 6 samples (H460 2D, H460 3D_SM, H460 3D_ FBS^low, MCF7 2D, MCF7 3D_SM, MCF7 3D_ FBS^low) were characterized through transcriptomic, proteomic and metabolomic analyses; differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) between 3D vs 2D samples were further analyzed by using Gene Ontology (GO). Integration: DEGs and DEPs were integrated to identify a common signature of DEGs and DEPs in all the 2D to 3D transitions. ALDOC and ENO2 were found up-regulated in all 3D vs 2D culture conditions. Validation: siRNA-mediated knock down of ALDOC and ENO2 were performed to functionally validate the effects of these two enzymes on 3D tumor spheroids growth. Output: ALDOC and ENO2 represent putative drivers of the metabolic reprogramming responsible for the sphere-forming ability of H460 and MCF7 cells