Fig. 7: Schematic model of tumour mass dormancy induction and exit phase regulated by β1 integrin. | Oncogene

Fig. 7: Schematic model of tumour mass dormancy induction and exit phase regulated by β1 integrin.

From: Emergence of β1 integrin-deficient breast tumours from dormancy involves both inactivation of p53 and generation of a permissive tumour microenvironment

Fig. 7

Schematic model highlighting the roles of β1 integrin receptors in regulating tumour mass dormancy induction and exit phase. In MIC WT model, β1 integrin suppresses p53 and Rb activities thereby allowing evasion of tumour suppressive barriers including cell cycle arrest, apoptosis, and cellular senescence. In contrast, β1 integrin deficiency reactivates those suppressive barriers, resulting the induction tumour mass dormancy. Tumour recurrence from dormancy exit requires both cell intrinsic (p53 alteration) and extrinsic events (CAF infiltration and ECM deposition). Potential factors mediating paracrine communication between cancer cells and fibroblasts are remained to be addressed. Created with BioRender.com.

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