High TAZ expression is associated with non-small cell lung cancer.

expression of miR-135b, LZTS1, LATS2 and nuclear TAZ predicts poor outcomes of non-small-cell lung cancer.

High TAZ expression is associated with non-small cell lung cancer.

Rottlerin exerted its tumor suppressive function via inactivation of TAZ in non-small cell lung carcinoma cells.

These results indicate that TAZ is an independent prognostic factor and plays an important role in Non-Small Cell lung cancer (NSCLC)progression and may serve as a novel therapeutic target of NSCLC.

this study identified TAZ as a novel inducer of lung cancer stem cells and the first transcriptional activator of the stem cell marker ALDH1A1

TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild-type non-small-cell lung cancer .

Nuclear TAZ activity associates with lung squamous cell carcinomas (LUSC). Nuclear TAZ activity correlates worse clinical outcomes in LUSC, suggesting a prognostic value for activated TAZ in LUSC. TAZ may be a valuable target for developing therapeutics treating LUSC.

TAZ might upregulate the expression of AREG, activate the EGFR signaling pathway and sensitize EGFR wild-type non-small-cell lung cancer to gefitinib.

A Division of Labor between YAP and TAZ in Non-Small Cell lung cancer.

TAZ negatively regulates the novel tumor suppressor ANKRD52 and promotes PAK1 dephosphorylation in lung adenocarcinomas.