Why is the Hippo pathway important?

Why is the Hippo pathway important?

The hippo pathway possesses the unique capacity to lead to tumorigenesis. Mutations and altered expression of its core components (MST1/2, LATS1/2, YAP and TAZ) promote the migration, invasion, malignancy of cancer cells.

What is cancer Yap?

Yes-Associated Protein (YAP) and Transcriptional Co-activator with PDZ-binding Motif (TAZ) are the downstream effectors of the Hippo signaling pathway that play a crucial role in various aspects of cancer progression including metastasis.

Is Yap a tumor suppressor gene?

These results suggest that YAP indeed acts as a tumor suppressor in lung SCC cells.

How is Hippo pathway activated?

Extensive studies have revealed a myriad of intrinsic and extrinsic signals that can activate the Hippo pathway, including cell–cell contact, stiffness of the extracellular matrix, stress signals, and cell polarity (reviewed in [2,11,32–34]).

Which protein controls hippo YAP pathway?

The Hippo core – regulation of LATS kinases LATS kinases are the key direct regulators of YAP proteins within the Hippo pathway. LATS kinases are activated by Ste20 family kinases, including Hippo, and its mammalian homologues MST1 and MST2 (collectively, Hippo kinases) (82).

How do you activate the Hippo pathway?

Is YAP an enzyme?

YAP1 was first identified by virtue of its ability to associate with the SH3 domain of Yes and Src protein tyrosine kinases. YAP1 is a potent oncogene, which is amplified in various human cancers….

YAP1
Location (UCSC) Chr 11: 102.11 – 102.23 Mb Chr 9: 7.93 – 8 Mb
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Is LATS1 an important tumor suppressor?

These results indicate that LATS1 is an important candidate tumor suppressor and its downregulated expression may contribute to glioma progression LATS1 phosphorylates a phosphatase as does the yeast Dbf2 and demonstrate a novel role of LATS1 in controlling PLK1 at the G2 DNA damage checkpoint.

How does LATS1 depletion affect cancer cell plasticity?

In contrast, LATS1 depletion augmented cancer cell plasticity, skewing luminal B tumors towards increased expression of basal-like features, in association with increased resistance to hormone therapy.

Is LATS2 down-regulated in Lumb breast cancer?

Here, we show that a LATS2-associated gene expression pattern is specifically down-regulated in lumB breast cancer. Deletion of Lats2 in the mouse mammary gland results in increased lumB tumorigenesis and metabolic rewiring of the tumor cells.

Do lats paralogs affect tumor suppression in breast cancer?

Concordantly, low LATS1 correlates with increased resistance to hormone therapy (tamoxifen). Thus, each LATS paralog exerts distinct tumor suppressive effects in the context of breast cancer, in a subtype-specific manner.

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