These results suggest that DUSP6 is a growth suppressor whose inactivation could promote the progression of lung cancer.

Dual specificity phosphatase 6 (DUSP6) is an ETS-regulated negative feedback mediator of oncogenic ERK signaling in lung cancer cells.

DUSP6 plays an important role in cancer resistance in different subtypes of non-small cell lung carcinoma.

High DUSP6 expression is associated with lung Squamous Cell Carcinoma.

DUSP6 rs2279574 SNPs was not associated with chemoradiotherapy response, whereas tumor regression, weight loss, clinical stage, and cigarette smoking were independent prognostic predictors for these Chinese patients with non-small cell lung cancer.

Individuals are carrying DUSP6 rs2279574 AA and AC genotypes associated with an increased risk in developing lung squamous carcinoma in Han Chinese and with advanced NSCLC stages.

A dual specificity phosphatase, DUSP6, that negatively regulates phosphorylation of (P)-ERK is up-regulated in EGFR- or KRAS-mutant lung adenocarcinoma (LUAD), potentially protecting cells with mutations in the RAS signaling pathway, a proposal supported by experiments with DUSP6-specific siRNA and an inhibitory drug

DUSP6 is a tumor suppressor in Non-small cell lung cancer.

DUSP6 protein expression was predominantly nuclear in breast CTCs and the brain metastases but not pleura or lung metastases of TNBC patients. Therefore, nuclear DUSP6 may play a role in the association with cancer spreading in TNBC patients, including brain metastasis.