Table 1 The pathways that could be activated by IFN-α2b
From: Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow
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] |