. 2018 Feb;15(1):14–28. doi: 10.20892/j.issn.2095-3941.2017.0107

2.

Role of DUSP6 and its outcome in different types of cancers.

Role of DUSP6	Cancer type	Outcome
Tumor-suppressive	Pancreatic cancer	DUSP6 reintroduction into pancreatic cancer cell line caused cell growth suppression & apoptosis in vitro⁷¹.
	Esophageal squamous cell & nasopharyngeal carcinoma	DUSP6 overexpression in ESCC & NPC cell lines impaired EMT-associated properties, cell migration & invasion suppression, and high E-cadherin expression ⁷⁴.
	Non-small cell lung cancer	Silencing of DUSP6 in lung cancer cell line caused ERK 1/2 activation & cellular proliferation increase, and meanwhile plasmid-driven DUSP6 overexpression caused ERK activation & cell proliferation reduction, & led to apoptosis ⁴⁰.
	Ovarian cancer	DUSP6 knockdown caused increase in ERK1/2 activation, cell proliferation, anchorage-independent growth ability & chemoresistance to cisplatin meanwhile enforced DUSP6 expression caused reverse effects ⁷³.
Tumor-promoting/ pro-oncogenic	Human glioblastoma	DUSP6 overexpression inhibited cell growth via G1-phase delay, increased anchorage-dependent growth & clonogenic potential in vitro, and chemoresistance to cisplatin⁷⁵.
	Thyroid carcinoma	PTC cell line & majority PTC and PDTC specimens showed DUSP6 overexpression due to BRAF, RET/PTC & TRK oncogenes activation, displaying tumor-promoting effect ⁶⁴.
	Breast cancer	DUSP6 silencing in MDA-MB-213 cell line caused decrease in cell proliferation, migration & invasion of cells, and cell growth arrest at G0/G1 phase while in MCF-7 cell line after PMA treatment, wild-type DUSP6 expression caused cell growth arrest, colony growth inhibition & stimulated invasive phenotype ⁷⁶.
	Acute myeloid leukemia (FLT3-ITD)	DUSP6 attenuation in 32D cell pools resulted in moderate impairment in proliferation and meanwhile forced exogenous DUSP6 overexpression in stable transfectant reduced in ERK1/2 phosphorylation but not cell proliferation⁷⁷.
Tumor-suppressive/tumor-promoting (depending on type of cell lines)	Melanoma	Tumor-promoting role: DUSP6 overexpression decreased ERK 1/2 phosphorylation, increased anchorage-dependent growth & invasion ability in immortal mouse melanocyte cell lines ⁸⁰. Tumor-suppressive role: DUSP6-transfected human melanoma cell line showed smaller & fewer anchorage-independent colonies and reduced invasive ability ^78,91.