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Cell Death Dis. 2018 May 1;9(5):517. doi: 10.1038/s41419-018-0548-3.

Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ.

Author information

1
Key Laboratory of Brain Functional Remodeling, Department of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, 107 Wenhua Xi Road, Jinan, Shandong, 250012, China.
2
Brain and Mind Centre, and Faculty of Health Sciences, University of Sydney, Camperdown, NSW 2050, Australia.
3
Department of Neurosurgery, Jining No.1 People's Hospital, Jiankang Road, Jining, 272011, China.
4
Key Laboratory of Brain Functional Remodeling, Department of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, 107 Wenhua Xi Road, Jinan, Shandong, 250012, China. jian.wang@uib.no.
5
Department of Biomedicine, University of Bergen, Jonas Lies vei 91, Bergen, 5009, Norway. jian.wang@uib.no.
6
Key Laboratory of Brain Functional Remodeling, Department of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, 107 Wenhua Xi Road, Jinan, Shandong, 250012, China. lixg@sdu.edu.cn.

Abstract

Increased Actin-like 6A (ACTL6A) expression has been implicated in the development of diverse cancers and recently associated with the Hippo signaling pathway, which is known to regulate biological properties, including proliferation, tissue regeneration, stem cell biology, as well as tumorigenesis. Here we first show that ACTL6A is upregulated in human gliomas and its expression is associated with glioma patient survival. ACTL6A promotes malignant behaviors of glioma cells in vitro and in orthotopic xenograft model. In co-immunoprecipitation assays, we discover that ACTL6A physically associated with YAP/TAZ and furthermore disrupts the interaction between YAP and β-TrCP E3 ubiquitin ligase, which promotes YAP protein degradation. Moreover, effects of ACTL6A on glioma cells proliferation, migration, and invasion could be mediated by YAP/TAZ. These data indicate that ACTL6A may contribute to cancer progression by stabilizing YAP/TAZ and therefore provide a novel therapeutic target for the treatment of human gliomas.

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