Table 1.

miRNAs and lncRNAs involved in regulation of NFAT5 expression and signalling pathways.

Cell Type/Disease	miRNA/lncRNA	Consequence	Reference
Adipocytes	miR-30b	miR-30b negatively regulates NFAT5. Upregulation of NFAT5 expression by knockdown of miR-30b contributes to the development of obesity and insulin resistance.	[19]
Renal medulla	-miR-466a-3p -miR-200b & miR-717	miR-466a-3p, miR-200b and miR-717 downregulate NFAT5 expression during osmotic response. High level of miR-466a-3p is associated with polydipsia, polyuria and disturbed ion balance.	[49,51]
HEK293 cells and human thymoma tissue	miR-20b	miR-20b contributes to the suppression of thymoma and thymoma-associated myasthenia gravis and inhibits T-cell activation and proliferation. The tumor suppressive function of miR-20b is via inhibiting NFAT5 expression.	[50]
Oral squamous cell carcinoma	miR-411-3p/lncRNA TTN-AS1	The lncRNA Titin antisense RNA 1 (TTN-AS1) acts as a miR-411 sponge, thereby inhibiting the miR-411 which is a negative regulator of NFAT5. Overexpression of NFAT5 restores cell growth in TTN-AS1 depleted cells.	[52]
Astrocytes	miR-218/lncRNA CCAT1	miR-218 targets NFAT5. The lncRNA colon cancer-associated transcript-1 (CCAT1) acts as a miR-218 sponge, thereby activating NFAT5 expression, which is crucial for controlling apoptosis and inflammation.	[53]
Cementoblasts	miR0361-3p	Overexpression of miR-361-3p suppresses cemantoblast differentiation through directly targeting NFAT5.	[54]
Mouse Ovarian granulosa	miR-27a	NFAT5 promotes cell proliferation through activating the Wnt signaling pathway. miR-27a directly inhibits NFAT5 expression. However, p53 negatively regulates miR-27a. Hence p53/miR-27a/NFAT5 pathway regulates mouse granulosa cell proliferation.	[55]
Myoblasts	miR-10b-5p	Knockdown of NFAT5 represses myoblast differentiation. miR-10b-5p regulates C2C12 myoblast differentiation and proliferation by directly targeting NFAT5 and repressing its activity.	[56]
T cells	-miR-106a, miR-18b and miR-363-3p -miR-181a -miR-568	A miRNA cluster of miR-106a, miR-18b and miR-363-3p is involved in the differentiation and function of T helper cells through directly inhibiting NFAT5. miR-568 affects the activation and function of CD4+ T cells and Tregs through targeting NFAT5. miR-181a enhances NFAT5 activation axis and is involved in regulating T-cell induction and autoimmunity linked to type 1 diabetes.	[57,58,59]
Macrophage	miR-223	PPARγ/miR-223 regulatory axis controls macrophage polarization through targeting downstream target genes such as NFAT5 and RASA1.	[60]
Sheep Wool follicle	miR-148b	miR-148b positively regulates proliferation of hair follicles through activating Wnt/β-catenin signalling pathway and inhibiting NFAT5.	[61]
Human primary glioblastoma	miR-641	miR-641 is tumor suppressive and negatively regulates the PI3K/Akt pathway via directly targeting several kinases and indirectly targeting NFAT5. miR-641 is downregulated in glioblastoma.	[62]
Glioblastoma cell & glioma samples	miR-338-3p/lncRNA SBF2-AS1	NFAT5 upregulates SBF2-AS1, which can sponge miR-338-3p, a negative regulator of EGFL7. Thus, NFAT5 promotes glioblastoma cell-driven angiogenesis via the SBF2-AS1/miR-338-3p/EGFL7 signaling pathway.	[63]
Hepatoma	miR-30e-5p	miR-30e-5p targets MAP4K4 to inactive MAPK and thereby suppresses NFAT5, which leads to promotion of HCC tumorigenesis via the oncogene DADS2 expression.	[64]
Microglia	miR-29c-3p	miR-29c-3p suppresses inflammasome activation via targeting NFAT5, impairing inflammatory response in Parkinson’s disease.	[65]