Table 1.

The pathways that could be activated by IFN-α2b

Cell type	Mechanism	Anticancer action	Notes	Citation
Jurkat, SupT1, H9, CEM, U937	Decreasing the phosphorylation level of MEK1/2 and ERK1/2	Inhibition of cell proliferation	Time-dependence, failure to function within a short period, functioning independently of the upstream signal of Ras and Raf-1	[33]
HepG2	Upregulating BECLIN1 and LC3-II	Induction of autophagy	NA	[34]
Kupfer cells, macrophages, liver parenchymal cells	Activating Caspase-3 and inducing the transport of pSMAD2/3 into nucleus	Induction of apoptosis	Validated in animal models	[35]
Liver parenchymal cells	Activating NADPH oxidase complex and inducing the production of reactive oxygen species	Induction of apoptosis	Validated in animal models	[36]
NA	Upregulting p53 and BAX and downregulating BCL-2 and BCL-xL	Induction of apoptosis	Validated in animal models	[37]
HepG2, Huh7	Downregulating HES1, HES7 and NOTCH1	Inhibition of cell proliferation and induction of cell cycle arrest	Using bone marrow mesenchymal stem cells that could express IFN-α2b protein	[38]
NCI-H295R	NA	Inhibition of cell proliferation and induction of cell cycle arrest and apoptosis	The required dose is too large. IFN-β might be a better choice	[39]
RPMI 8226, U266, NCI-H929	Upregulating TRAIL	Induction of apoptosis	Functioning after 72 h. The function could be antagonized by G1P3 within a short period	[40]
KB	Activating PARP-1	Inhibition of cell proliferation and induction of cell cycle arrest and apoptosis	NA	[41]
SK-MEL-3, SK-MEL-28	Upregulating TRAIL	Induction of apoptosis	Hypermethylation of TNFRSF10A gene could impair the function of IFN-α2b	[42]