YAP inhibits squamous transdifferentiation of Lkb1-deficient lung adenocarcinoma through ZEB2-dependent DNp63 repression.

The findings identify YAP as an important contributor to lung cancer progression, rationalizing YAP inhibition in the context of LKB1 deficiency as a therapeutic strategy to treat lung adenocarcinoma.

claudin family member highly expressed in lung alveolar epithelium, leads to lung enlargement, parenchymal expansion, increased abundance and proliferation of known distal lung progenitors, the alveolar epithelial type II (AT2) cells, activation of Yes-associated protein (YAP), increased organ size, and tumorigenesis in mice

Results suggest that YAP1 may play an important role in prognosis of small-cell lung cancer patients treated with platinum-based chemotherapy.

the transcriptional coactivator YAP1 was determined to be a direct target of miR-375 in lung cancer cells

Over-expression of YAP was associated with non-small cell lung cancer, especially lung adenocarcinoma.

Results implicate YAP1 R331W as an allele predisposed for lung adenocarcinoma with high familial penetrance.

our study is the first to indicate the potential role of YAP1 as a common modulator of resistance mechanisms in lung cancer

YAP may act as an oncogene and predict poorer prognosis in well differentiated lung adenocarcinoma.

Collectively, we suggest a novel EGFR-TKI resistance mechanism involving YAP activation and suggest targeting YAP and EGFR simultaneously may be a breakthrough treatment of primary and acquired EGFR-TKI resistant lung cancer.

miR-138 may play a suppressive role in the growth and metastasis of non small cell lung cancer cells partly at least by targeting YAP1

Our results indicate that YAP promotes erlotinib resistance in the erlotinib-sensitive non-small cell lung cancer cell line HCC827

Results show that MiR-424-3p directly and negatively regulates YAP1 in non-small cell lung cancer cells through binding its 3'-untranslated region.

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

Results found YAP1 overexpressed in lung cancer side population cells. YAP1 regulates ABCG2 at the transcriptional level through binding to the promoter of ABCG2. The study adds a new function for YAP1 that may be relevant to drug resistance and cancer therapy through regulation of ABCG2 and side population cell formation in lung cancer.

Study demonstrates for the first time that S100A7 not only functions as a facilitator of adenous-squamous carcinoma phenotypic transition in lung cancer cells but also that its expression is differentially regulated by the Hippo-YAP pathway.

Authors discovered that lung cancer cells survive initial EGFR inhibitor treatment through activation of not only STAT3 but also Src-YAP1 signaling.

Study suggestes that Rab11a serves as an important oncoprotein and a regulator of YAP in human non-small cell lung cancer.

The Hippo effector YAP plays a crucial role in linking the PD-L1 and EGFR-TKI resistance by directly regulating the expression of PD-L1 in lung cancer cells.

miR-361 targets 3'UTR of YAP mRNA to depress the proliferation of lung cancer cells

we identified YAP-driven AXL overexpression as a mechanism of resistance to EGFR TKIs in lung cancer cells.

These observations revealed the importance of YAP in promoting TKI-resistance and combined YAP inhibition can be a potential therapy delaying the occurrence of TKI-resistance in lung adenocarcinoma.

Data show that YAP1 is actively involved in initiation, progression, and metastasis of lung cancer. Further results not only implicates that YAP1 contributes to the maintenance of cancer stem-like cell activities, but also reveals a feed-forward relationship between YAP1 and FGFR1 signaling pathways in human lung cancer cells.

our results suggest that YAP plays an important role in promoting lung adenocarcinoma brain metastasis and that direct inhibition of YAP by shRNA suppresses H2030-BrM3 cell brain metastasis in a murine model.

Up-regulation of COPB2 inhibited cell apoptosis and promoted cell growth and tumorigenesis through up-regulating YAP1 expression in lung adenocarcinoma.

LOX nuclear localization was significantly associated with poor survival in patients with Colorectal cancer (CRC). Nuclear LOX expression was correlated with synchronous or postoperative lung/hepatic metastasis. LOX may prove to be a potential target gene of YAP and TEAD4.

An inverse correlation between the miR5063p and YAP1 mRNA levels was detected in lung adenocarcinoma specimens.

MicroRNA-345 suppresses cell invasion and migration in non-small cell lung cancer by directly targeting YAP1.

High YAP1 expression is associated with lung adenocarcinomas.

YAP1 promotes multidrug resistance of small cell lung cancer by CD74-related signaling pathways.

TM4SF1 facilitates non-small cell lung cancer progression through regulating YAP-TEAD pathway.

ANKHD1 promotes proliferation and invasion of nonsmallcell lung cancer cells via regulating YAP oncoprotein expression and inactivating the Hippo pathway.

MicroRNA-16 inhibits the proliferation and metastasis of human lung cancer cells by modulating the expression of YAP1.

Hippo pathway and tumoral FOXP3 expression correlate with tumor growth in squamous cell carcinoma of the lung.

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