17q25.3

Colorectal carcinoma

SLC16A3/MCT4 protein is overexpressed in colorectal cancer (Pinheiro et al., 2008a).

Cervical cancer

SLC16A3/MCT4 protein is overexpressed in cervical cancer (Pinheiro et al., 2008b). SLC16A3/MCT4 protein overexpression in cervical cancer correlated with positivity for high-risk HPV (Pinheiro et al., 2008b).

Bladder cancer

SLC16A3 gene expression was upregulated in some bladder tumours and induced by hypoxia in bladder cancer cell lines, but not in cultures of normal urothelium (Ord et al., 2005).

Breast cancer

Induction was also seen in two breast cancer cell lines. Expression of SLC16A3 gene is higher in breast cancer distant metastasis as compared to primary tumours or regional metastasis. SLC16A3 gene was then included in the VEGF profile of breast cancer, associated with promotion of vessel formation, survival under anaerobic conditions and loss of dependence upon fibroblasts (Hu et al., 2009).

Ovarian cancer

SLC16A3 gene expression was described to be downregulated in malignant ovarian tumours as compared to normal ovarian surface epithelial cells. Additionally, the non-tumorigenic cell line TOV-81D presented higher expression that tumorigenic cell lines (Wojnarowicz et al., 2008).
SLC16A3 gene, among other transporter genes, was differentially expressed in a chemotherapy resistant ovarian cancer cell line and tumour tissue as compared to a chemosensitive cell line and tumour tissue. It was suggested that these transporters might be involved in drug influx/efflux, modulating chemotherapy response (Cheng et al., 2010).

Mitochondrial myopathy

SLC16A3/MCT4 overexpression was described in a patient with a mitochondrial myopathy (Baker et al., 2001).

Chronic obstructive pulmonary disease

SLC16A3/MCT4 downregulation was described in the vastus lateralis muscle of patients with chronic obstructive pulmonary disease as compared with healthy controls (Green et al., 2008).