TABLE 2.

Multiple miRNAs are shown to regulate SLC16A1/MCT1.

Transporters	Endogenous substrates	miRNAs	Diseases and/or model systems	Observations	References
SLC16A1/MCT1	L-lactic acid Pyruvic acid β-D-hydroxybutyric acid	miR-124-3p	Medulloblastoma cell lines D283, D341, D384, D425, D458, DAOY, and ONS-76 cells	Transfection with miR-124 mimics reduced SLC16A1 protein by 70% in DAOY cells and over 90% in the other medulloblastoma cell lines	Li et al. (2009)
			29 clinical medulloblastoma samples
		miR-29a-3p, miR-29b-3p, and miR-124-3p	Pancreatic beta cell line MIN6, hepatoma cell line mhAT3F, and HEK293 cell lines	miR-29b overexpression significantly downregulated SLC16A1 protein, while miR-29a and miR-124 overexpression almost eliminated SLC16A1 protein expression	Pullen et al. (2011)
			C57BL/6 mice
		miR-342-3p	Triple negative breast cancer	miR-342-3p overexpression caused SLC16A1 protein levels to be 50% of the control in MDAMB468 cells, 64% in BT549 cells, 38% in Sum149 cells, 73% in SUM159, but did not cause downregulation in MDAMB157 cells	Romero-Cordoba et al. (2018)
			Breast cancer cell lines MDAMB468, BT549, SUM159, MDAMB157 cell lines
			164 clinical breast cancer samples
			TCGA and METABRIC data sets