Table 2.

Expression of miRNA and lncRNA in control and cancer. Low and high expression are indicated by “−” or “+”, respectively. Mechanisms linking cancer and NO are also specified.

		Type of Cancer	Expression		Molecular Mechanism	Interaction with NO	Impact of the Regulatory Mechanism in Carcinogenesis		References
			Control	Cancer
miRNAs	miR-29b/c	Gastric cancer	−	+	Expression of miR-29b/c is regulated by NOS2	Not specified	NOS2↑–miR-29b/c↑–PTEN↓-Migration↑–Apoptosis↓	NOS2 regulates the expression of miR-29b/c, which in turns reduces PTEN and apoptosis, and increases migration	[92,93,94]
	miR-335, miR-543	Prostate cancer/ Liver cancer	+	−	Post-transcriptional regulation of NOS3	NOS3 mRNA degradation (miRNA target)	miR-335, miR-543↓–NOS3↑–Metastatic potential↑	miR-335 and miR-543 target NOS3 mRNA for degradation. In cancer, downregulation of these miRNAs, increases NOS3 expression leading to higher metastatic potential	[95,96]
	miR-193b	Breast cancer	+	−	Post-transcriptional regulation of NOS2 regulator DDHA1	DDHA1 mRNA degradation (miRNA target)	miR-193↓–DDAH1↑–ADMA↓–NOS2↑–Angiogenesis↑	Downregulation of miR-193b reduces DDAH1 mRNA degradation, which increases ADMA elimination and consequent increased NOS2 activity. This leads to increased angiogenesis	[97]
	miR-16	Pan-cancer (macrophages)	+	−	NO production	Not specified	miR-16↓–NO production↓–Pro-tumoral microenvironment↑ and miR-16↓–PD-L1↑–Pro-tumoral microenvironment↑	miR-16 in M1 macrophages is able to increase NO production, leading to an anti-tumoral microenvironment. Also, miR-16 targets PD-L1 mRNA for degradation, leading to reduced immunosuppression. In M2 macrophages, downregulation of miR-16 coincides in reduced NO production	[99]
	miR-155	Pan-cancer (macrophages)	+	−	Post-transcriptional regulation of NOS2	Not specified	miR-155↓–NOS2↓–FGF2↑–Proliferation↑	Downregulation of miR-155 decreases NOS2 expression and increases FGF2, promoting tumor proliferation	[100]
	miR-155	Liver cancer	−	+	Exogenous NO increases miR-155 expression	Not specified	miR-155↑–tumor suppressor gene P21WAF/CIP1↓	In liver cancer, upregulation of miR-155 by exogenous NO donors, blocks tumor suppressor gene P21WAF/CIP1	[102,103]
	miR-204	Acute myeloid leukemia	+	−	Post-transcriptional regulation of SIRT1, NOS2 and COX2	Not specified	miR-204↑–SIRT1↓/NOS2↓/COX2↓	In AML cells, miR-204 reduces expression of SIRT1, COX2 and NOS2 exerting proapoptotic and antiproliferative properties	[118]
	miR-939-5p	Triple-negative breast cancer	+	−	Post-transcriptional regulation of NOS2	Not specified	miR-939-5p↑–NOS2↑–NO↑	miR-939-5p downregulates NOS2 expression in cultured human hepatocytes and in TNBC	[119]
	miR-148b-3p	Liver cancer (Hepatic sinusoidal endothelial cells)	+	−	Post-transcriptional regulation of NOS3 and NOX4	NOX4 mRNA degradation (miRNA target)	miR-148b-3p↑–NOS3↑/NO↑–NOX4↓	miR-148b-3p regulates negatively NOX4, it also enhances NOS3 expression and NO production in HSEC	[120]
	miR-122	Liver cancer	+	−	Post-transcriptional regulation of SLC7A1 arginine transporter	SLC7A1 mRNA degradation (miRNA target)	miR-122↓–SLC7A1↑–Arginine↑–NO production↑–Cell proliferation↑	Downregulation of miR-122 promotes cell proliferation in liver cancer through upregulation of NO production. In particular, miR-122 targets arginine transporter SLC7A1. Under circumstances of reduced expression of miR-122, SLC7A1 is not degraded and arginine availability increases	[104]
lncRNAs	UCA1	Acute myeloid leukemia	−	+	Post-transcriptional regulation	miR-204 mRNA degradation	UCA1↑–miR-204↓–SIRT1↑/NOS2↑/COX2↑	UCA1 downregulates miR-204 expression and it enhances expression of SIRT1, NOS2 and COX2	[118]
	HEIH	Triple-negative breast cancer	−	+	Post-transcriptional regulation	miR-939-5p degradation	HEIH↑–miR-939-5p↓–NOS2↑–NO↑	In TNBC HEIH decreases miR-939-5p expression, which consequently enhances NOS2 expression and NO production	[119]
	H19	Liver cancer (Hepatic sinusoidal endothelial cells)	−	+	Post-transcriptional regulation	miR-148b-3p degradation	H19↑–miR-148b-3p ↓–NOS3↓/NO↓–NOX4↑	H19 negatively regulates miR-148b-3p, so it turns to downregulate NOS3/NO and upregulates its direct target NOX4 in HSEC	[120]