Several reports are there that mammalian reproductive fluids contain some factors, which cause quiescence of sperm.
By inducing cytostatic levels of p53 and causing quiescence, we can protect normal cells from chemotherapy, without protection of cancer cells lacking p53.
Second, p53 inhibits mTOR-centric network and this can prevent senescence, causing quiescence instead.
While inhibiting mTOR, p53 suppressed p21-induced senescence, causing quiescence instead [ 27]. p53 affects autophagy and metabolic pathways not only via inhibition of mTOR but also probably independently from mTOR [ 22, 28- 35].
This exciting but rather heretic hypothesis was based on initial observations showing that senescent phenotype requires cell growth [ 8, 9]and that, unlike ectopic p21 expression or DNA damage by doxorubicin, p53 induction caused quiescence instead of senescence in some cells [ 10].
Withdrawal of growth factors causes quiescence: the quiescent cell neither grows, nor cycles, and its functions and metabolism are low.
Further, exposure of hNPCs to HIV-1 causes quiescence of NPCs, through engagement of the chemokine receptor CXCR4 (for receptor nomenclature see Alexander et al., 2013; Krathwohl and Kaiser, 2004).
Moreover, we recently reported that in human fibroblasts (WI-38tert) and fibrosarcoma cells (HT-1080-p21-9), in which nutlin-3a caused quiescence [ 16], p53 acted as a suppressor of senescence [ 17].
But rapamycin does not induce proliferation and in contrast can cause quiescence (in some cell types).
It was assumed that when p53 causes quiescence, it simply fails to induce senescence.
