Kaarin Wasland's research while affiliated with NorthShore University HealthSystem and other places

... This suggests a functional effect of the rs3890158 SNP, likely mediated by the FOXO3 transcription factor. Snoeks et al. [43] have shown that TNF-a induces the translocation of nuclear FOXO3 into the cytosol where it undergoes proteasomal degradation in human intestinal HT-29 cells. The interpretation of our results is consistent with the higher expression of IL8RB in gastric cancer tissues than in adjacent noncancerous tissues , given that IL8RB positively regulates the migration and invasion abilities of gastric cancer cells, which are characteristics of the malignant tumor [44]. ...

... In a mechanistic study of genistein, it was revealed that Akt inhibition causes decreased telomerase enzyme activity as well as an elevated level of cell cycle progression inhibitor (i.e., p27) leading to apoptosis activation in breast cancer (Chinni et al. 2003). Similarly, genistein inactivates Akt protein in colon cancer cells via stimulation of the Foxo3 transcription factor that finally increased the p27 expression levels (Qi et al. 2011). Recently, genistein plus centchroman inhibited the phosphorylation of PI3K, NF-κB, and Akt which subsequently promoted apoptosis in breast adenocarcinoma by following events such as PARP cleavage, elevated Bax/ Bcl 2 ratio, and stimulation of caspases 3 and 9 (Kaushik et al. 2019). ...

... Of special pathophysiological relevance, the FAs released from LDs are not only used for energy production, but also act as signaling molecules (e.g., lysophosphatidic acid) regulating tumor progression and metastasis [460,467]. Furthermore, LDs are able to modulate cell cycle checkpoints and gene expression in tumor cells (e.g., G 0 /G 1 bypass and regulation of FOXO3A activity) [460,468,469]. In addition, LDs also enable the intracellular trafficking of growth-signaling proteins such as PI3K, ERK1, ERK2, p38, and PKC, as well as endo-/transcytosis-regulating caveolin, which are also involved in tumorigenesis [470,471]. ...

... The diseases and functions associated with these DEGs include gastrointestinal disorders, metabolic diseases, lipid metabolism, immune responses, immune cell trafficking, inflammatory pathways, and cancer ( Figure 3A). To determine the contribution of loss of FOXO3 in PMNs to colonic pathobiology, their upstream regulators of DEGs were identified and compared to transcriptomes from the total colonic tissue of FOXO3-deficient mice, which has exacerbated inflammatory and tumorigenic processes [27,35,42]. We found substantial similarities in upstream regulators of DEGs associated with FOXO3 KO PMNs and total FOXO3 KO colon, which were related to lipid metabolism (eicosapentenoic acid, LEP), immune response (CD40LG, CpG oligonucleotide), inflammatory pathways (SIRT1, HNF-4α), and tumorigenesis (NUPR1, ID1, CREB1, CBFB) ( Figure 3B). ...

... Previously, we demonstrated that BFT exposure in IECs provokes specific signaling pathways that eventually result in the activation of transcription factors such as NF-κB and AP-1 [14][15][16]. Since early work revealed that lipopolysaccharide (LPS) and infection with Citrobacter rodentium target the FoxO3a transcription factor in intestinal epithelia [38], we hypothesized that BFT-induced autophagy requires FoxO3a in IECs. In the present study, the increased expression of FoxO3a by BFT treatment was observed in the nuclear fraction of HCT-116 cells. ...