Regulators of mammalian Hippo pathway in cancer

Liu, Angela M.; Wong, Kwong-Fai; Jiang, Xiaoou; Qiao, Yiting; Luk, John M.

doi:10.1016/j.bbcan.2012.05.006

Cited by 43 publications

(38 citation statements)

References 110 publications

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“…The core components of Hpo pathway include Hpo, Warts, Sav and Mats, all of which are highly conserved ( Figure 2). 16 MST1 and MST2, which are highly abundant in lymphoid tissues, are mammalian homologs of drosophila 'Hpo'. Sav, Ras-association domain family protein (Rassf), and Hpo share similar dimerization regions called SARAH domains.…”

Section: Gck-ii Kinases Regulate Lymphocyte Adhesion Migration Prolmentioning

confidence: 99%

Germinal center kinases in immune regulation

Yin

Shi

et al. 2012

Cell Mol Immunol

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Section: Gck-ii Kinases Regulate Lymphocyte Adhesion Migration Prolmentioning

confidence: 99%

Germinal center kinases in immune regulation

Yin

Shi

et al. 2012

Cell Mol Immunol

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“…Recently, LATS2 has been shown as a negative regulator of Hippo/Yap signaling [19]. Inactivation of LATS2 led to the overgrowth of the cells and ultimate tumorigenesis [19,20]. Given our observations that LATS2 negatively regulated NF-κB signaling, it is very interesting to investigate the cross talk between NF-κB and Hippo/ Yap signaling in the context of LATS2 inactivation in NSCLC.…”

Section: Discussionmentioning

confidence: 92%

LATS2 inhibits the activity of NF-κ B signaling by disrupting the interaction between TAK1 and IKKβ

et al. 2015

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NF-κB signaling plays very important role in the tumorigenesis of nonsmall cell lung cancer (NSCLC). However, the molecular mechanisms for the dysregulation of NF-κB signaling in NSCLC have not been fully understood. In the previous reports, we have showed that large tumor suppressor gene 2 (LATS2) inhibited NF-κB signaling in NSCLC cells, whereas the details for the mechanism remain unknown. Here, we reported that LATS2 is a suppressor of tumor necrosis factor (TNF-α)-induced NF-κB signaling by inhibiting the interaction between TAK1 and IKKβ. Overexpression of LATS2 largely blocked TNF-α-induced NF-κB activation and IκBα degradation, whereas knockdown of LATS2 showed the opposing results. Mechanistically, we identified that LATS2 interacted with IKKβ and blocked the interaction between IKKβ and TAK1. Our results indicate that LATS2 functions as a pivotal negative regulator in TNF-α-induced activation of NF-κB via disrupting the interaction of TAK1 with IKKβ.

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“…The Hippo signaling pathway regulates the organ size in various species, and dysregulation of this pathway may induce the development of tumors (18). Since the disruption of any factor in this pathway can lead to tumorigenesis, YAP is recognized as an oncogene and the major downstream effector of the Hippo signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of YAP inhibits proliferation and induces apoptosis in Eca‑109 cells

Cui

2017

Exp Ther Med

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Abstract.A previous study reported that Yes-associated protein (YAP) gene was overexpressed in esophageal squamous cell carcinoma (ESCC); however, the exact role of YAP in ESCC remains largely unclear. The present study aimed to investigate the effects of YAP inhibition on ESCC. In order to investigate the exact role of YAP in ESCC cells, a stable YAP low-expression ESCC cell line was established using YAP-small interfering RNA. MTT assay was performed to examine the cell proliferation ability, while flow cytometry were used to detect the cell apoptosis and cell cycle distribution. In addition, reverse transcription-quantitative polymerase chain reaction and western blot analysis were applied for mRNA and protein level detection, respectively. The results suggested that YAP gene inhibition significantly repressed the ECA-109 cell proliferation and induced cell apoptosis, whereas this inhibition had no significant effects on cell cycle. Furthermore, the expression levels of cell apoptosis-associated proteins were determined in the current study, and the data demonstrated that the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and phosphorylated extracellular signal-regulated kinase expression were significantly reduced, while the p53 and caspase 3 levels were notably increased in YAP gene-inhibited ECA-109 cells. In conclusion, the current study revealed that YAP gene inhibition suppresses the proliferation and induces apoptosis in ECA-109 cells, indicating that the YAP gene serves as an oncogene in ESCC.

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Regulators of mammalian Hippo pathway in cancer

Cited by 43 publications

References 110 publications

Germinal center kinases in immune regulation

Germinal center kinases in immune regulation

LATS2 inhibits the activity of NF-κ B signaling by disrupting the interaction between TAK1 and IKKβ

Downregulation of YAP inhibits proliferation and induces apoptosis in Eca‑109 cells

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