Table 3.

Therapeutic strategies against quiescence

Type of cancer	Therapeutic target	Potential therapy	Therapeutic mechanism
AML	HDM2	PNC-27	PNC-27 binds to mHDM2, leads to E-cadherin degradation, and causes membrane injury and cell necrobiosis[140]
AML	EVI-1	ATRA	ATRA enhances EVI-1-dependent depression of the maturation and promotes the quiescence[141,142]
AML	c-MPL	AMML2	AMML2 blocks c-MPL, stimulates entry of quiescent LSCs into the cell cycle, and increases the sensitivity of LSCs to chemotherapy[143]
AML	EZH1, EZH2	OR-S1, OR-S2	OR-S1 and OR-S2 inhibit EZH1/2, inactivate PRC2, and then eliminate quiescent LSCs, induce cell differentiation, and turn chemotherapy-resistant LSCs into a chemotherapy-sensitive population[145]
CML	Autophagy	Lys05, PIK-III	Lys05 achieves autophagy inhibition in LSCs and promotes differentiation; Lys05 and PIK-III inhibit TKI-induced autophagy and increase the sensitivity of LSCs to TKI[146]

AML: Acute myeloid leukemia; CML: Chronic myelogenous leukemia; LSC: Leukemia stem cell.