Fig. 3

Mechanisms of various dormancy inducers in cancer cells. A Noncoding RNAs, including ELEANORs and miR197, regulate dormancy-inducing gene expression in the nucleus and cytoplasm, respectively. The ELEANORs bind transcription factors to promote gene expression, and miR197 suppress target mRNA expression. B Various axis and signaling pathways that participate in regulatory mechanisms to induce dormancy. STAT1 is activated by chemotherapy, promoting IRF7 transcription, which stimulates IFN-β that activates CD4 + and CD8 + T cells. FAO pathway increases ACLY to elevate the levels of acetyl-CoA, which activates the transcription factor p300 to promote the transcription of NANOG and enhance the activation of factors that induce cancer cell dormancy. CCL2 and SAA2 transcribed under CXCL12 stimulation. WNT5A activates SIAH2 via ROR2, subsequently inhibits β-catenin signaling. TGFβ2 activates p38 to translocate to promote the transcription of NR2F1. The elevated NR2F1 leads to increased levels of SOX9 and RARβ. PKD1 promotes CREB1 phosphorylation to translocation, which activates the transcription of GAS6. Transcription of BHLHE41 is enhanced via p38 cascade, which increased p53 as a consequence. C Maintenance of cancer dormancy is influenced by hypoxic conditions and the ECM. Dormant or proliferative condition can be sustained under low or high oxygen levels, and ECM tightness surrounding cancer cells affect oxygen permeability. D 5-Aza-C induces histone modifications H3K4me3 and H3K27ac promotes the transcription of NR2F1 and leads to cancer cell dormancy