Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Table 1 Therapeutic options based on c-MYC targeting are represented by various strategies in inflammatory and cancerous colonic disorders

Main mode of action	Potential pathways/agents
Inflammatory colonic disorders
Upregulation of c-MYC expression	GSK inhibitors ± MSCT
Inhibition of c-MYC signaling	BET inhibitors ± c-MYC inhibitors
(suppression of Th1 function)
Cancerous colonic diseases
Downregulation of c-MYC expression	dose-dependent gene and protein expression suppression; PPAR-γ (5-ASA, mesalazine)
	suppressing protein expression by UDCA
	crosstalk with integrins
	E2F1 inhibition (downregulatin GCN5 expression)
	FGFR kinase inhibition
	epigenetic regulation by miR-320b
	siRNA blocking of ABC-transporters
	lncRNAs (blocking of PARROT or CCAT1-L)
	siRNAs using PEI-PGMA platform
	modified ODC promoter
Promoting c-MYC degradation	26S proteosomal pathway (aspirin)
	SIRT2 inhibition
Inhibition of c-MYC signaling	Omomyc
	BET (+ Wnt/MAPK) inhibitors

GSK: Glycogen synthase kinnase; MSCT: Mesenchymal stem cell transplantation; PPAR-γ: Peroxisome proliferator-activated receptor-γ; 5-ASA: 5-aminosalicylate; UDCA: Ursodeoxycholic acid; E2F1: E2F Transcription factor 1; GCN5: Histone acetyltransferase; FGFR: Fibroblast growth factor receptor; miR-320b: Micro-ribonucleic acid-320b; siRNA: Small interfering ribonucleic acid; ABC: Adenosine triphosphate-binding casette; lncRNA: Long noncoding ribonucleic acid; PARROT: Proliferation associated RNA and regulator of translation; CCAT1-L: Longer isoform of colon cancer associated transcript 1; PEI-PGMA: Polyethileneimine-polyglycidal methacrylate; ODC: Ornithine decarboxylase; SIRT2: Sirtuine2; BET: Bromo- and extra-terminal domain; MAPK: Mitogen-activated protein kinase.