TABLE 2.

Selected signaling pathways and transcription factors involved in CKD related to carcinogenesis.

Pathways/transcription factors	Animal model/cell analyzed	Indications	Results	References
ROS/Src/FAK	Human bladder cancer cells	Uremic toxin P-CS could induce bladder cancer cell migration and EMT through ROS/Src/FAK signaling pathway	Bladder cancer	Peng et al., 2020
Nrf2-NF-κB	In vivo: patients on hemodialysis (HD)	Oxidative stress in CKD patients resulted in a downregulation of the antioxidant effect of the Nfr2 system as well as an upregulation of oxidative regulation triggered by concomitant NF-κB activation, which might be associated with certain T cell lymphoma	T cell lymphoma	Pedruzzi et al., 2015; Giri and Aggarwal, 1998
	In vitro: RAW 264.7 macrophage-like cells
ADAM-17/TGF-α/EGFR	Human proximal tubule epithelial cells	Activation of EGFR might indirectly regulate CCL-2 and CCL-5 expression to induce tumors	Prostate, gastric and colorectal cancers	Morgado-Pascual, et al., 2015; Yamaguchi et al., 2021
AHR	In vivo: CKD patients; mice modal of CKD	Uremic toxin might activate AHR in CKD to participate in pro-tumor effects	Hodgkin’s lymphoma, chronic lymphocytic leukemia, adult T-cell leukemia, and cancers of the breast, head and neck, brain, kidney, lung, pancreas, and gastrointestinal tract	Dou et al., 2018; Wang et al., 2020b
Wnt/β-catenin	CKD patients	Inflammatory/oxidative processes are accompanied by activation of the Wnt/β-catenin signaling pathway, and the activated Wnt/β-catenin signaling pathway is involved in the development and progression of solid tumors and hematologic malignancies	Hepatocellular carcinoma and multiple myeloma	Chen et al., 2017; He and Tang, 2020; Hu and Hu, 2018