
pmid: 28935017
pmc: PMC5973372
Lung cancer is the leading cause of cancer related mortality in the world, with more than 1 million deaths per year, accounting for about one fifth of all cancer deaths worldwide. Over the past years, lung cancer treatment has been based on surgery, radiation therapy, chemotherapy, targeted therapies, and immunotherapy, but the improvement is not very perfect. Therefore, it has become clear that additional therapeutic strategies are urgently required to provide an improved survival benefit for patients. In recent years, Hippo signaling pathway has become a popular direction in the field of cancer research. When the Hippo pathway is active, the core Hippo kinase, such as MST/MOB and LATS1/2, inhibit the two transcriptional co-activators, YAP/TAZ. And YAP/TAZ are phosphorylated and sequestered in the cytoplasm. Dysregulation of the Hippo pathway drives multiple aspects of lung tumor initiation and progression. Moreover, the potential value of this pathway is getting more and more prevalent in clinical application. In this review, we summarize the molecular mechanism and the core components, upstream or downstream targets of Hippo signaling pathway which contribute the formation of lung cancer and discuss the therapeutic potential of targeted strategies in lung cancer. Additionally, we highlight the prospect of research on Hippo signaling pathway in the future.
Lung Neoplasms, Progression, Tumor Suppressor Proteins, Intracellular Signaling Peptides and Proteins, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Protein Serine-Threonine Kinases, Lung neoplasms, Animals, Humans, Hippo signaling pathway, RC254-282, Adaptor Proteins, Signal Transducing, Signal Transduction
Lung Neoplasms, Progression, Tumor Suppressor Proteins, Intracellular Signaling Peptides and Proteins, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Protein Serine-Threonine Kinases, Lung neoplasms, Animals, Humans, Hippo signaling pathway, RC254-282, Adaptor Proteins, Signal Transducing, Signal Transduction
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