Abstract
The connection between indoleamine 2,3-dioxygenase 1 (IDO1) and tumour dormancy – a quiescent state of tumour cells which has been consistently linked to metastasis and cancer recurrence – is rarely discussed despite the pivotal role of IDO1 in cancer development and progression. Whilst the underlying mechanisms of IDO1-mediated dormancy are elusive, we summarize the IDO1 pathways which potentially contribute to dormancy in this review. Critically, distinct IDO1 activities are involved in dormancy initiation and maintenance; factors outside the well-studied IDO1/kynurenine/aryl hydrocarbon receptor axis, including the mammalian target of rapamycin and general control nonderepressible 2, appear to be implicated in dormancy. We also discuss various strategies for cancer treatment via regulating IDO1-dependent dormancy and suggest the application of nanotechnology to deliver effective treatment.
Highlights
Cancer cells often remain unaltered and hidden until appropriate conditions for further progression are met
It should be noted that there are other enzymes, including tryptophan-2,3-dioxygenase and IDO2, which are closely related to IDO1, yet they could have complementary or differential roles during immunosuppression: TDO triggers the same Kyn/aryl hydrocarbon receptor (AhR) downstream signalling with IDO1 that they show nearly identical bioactivity [76]; IDO2 is documented to implement in the IDO1-dependent regulation of T cells [77], but it is reported that IDO1 and IDO2 may show opposite roles in immune responses [78]
Previous literature has suggested IDO1 should be connected to immunosuppression and tumour dormancy
Summary
Cancer cells often remain unaltered and hidden until appropriate conditions for further progression are met. IDO1 inhibition has, been proposed as a potential strategy to break dormancy, promote tumour suppression, and simultaneously improve other anti-cancer treatments, including chemotherapy. Through the IDO1/Kyn/aryl hydrocarbon receptor (AhR) metabolic cascade, IFN-g upregulates p27 to suppress the JAK/ STAT signalling and simultaneously induces G0/G1 cell cycle arrest in TRCs [11].
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