PAK6

Official Full Name

p21 (RAC1) activated kinase 6

Organism

Homo sapiens

GeneID

56924

Background

This gene encodes a member of a family of p21-stimulated serine/threonine protein kinases, which contain an amino-terminal Cdc42/Rac interactive binding (CRIB) domain and a carboxyl-terminal kinase domain. These kinases function in a number of cellular processes, including cytoskeleton rearrangement, apoptosis, and the mitogen-activated protein (MAP) kinase signaling pathway. The protein encoded by this gene interacts with androgen receptor (AR) and translocates to the nucleus, where it is involved in transcriptional regulation. Changes in expression of this gene have been linked to prostate cancer. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Dec 2015]

Synonyms

PAK5;

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Detailed Information

PAK6 roles as a potential anti-cancer target

In subsequent to the first discovery of PAKs in designing novel antifungal agents by Manser and colleagues, its biology has attracted significant attention in the ensuing decades. In group II PAKs, PAK6 is less characterized than other members, and studies on its role as an interesting partner of AR in prostate cancer cells have been a focus since confirmed to be independent of Rho GTPases. As a 681 amino acid protein with a molecular mass of 75kDa, PAK6 is located on chromosome 15q15, its gene is at the length of 38kb and comprised of 17 transcripts. The existence of a conserved N-terminal CRIB and a C-terminal kinase catalytic domain is similar to other members of the PAK family. Be similar to the CRIB domains of the previously characterized PAKs, the N-terminus of PAK6 consisted by six of the eight common CRTB domain residues. And C-terminal of PAK6 share more than 50% similarity with PAK1-3 in sequence and 80% homology to PAK4, it may reflect the alternative mechanisms of kinase regulation.

PAK6 has been shown to be either deregulated or hyper-activated in a large number of human cancers in recent years, more than this, it has been shown with essential relatedness with many fundamental cellular processes typically deregulated in cancer, such as cell migration, differentiation, and survival. Aberrant expression of PAK6 in a large number of human diseases, including cancer, has been underpinned by accumulating data. For its function, even though there is a reasonable understanding of the signal-framework, some basic problems remain elusive. Different PAKs perform different or even opposite functions during cancer development while most are considered oncogenes. It may be the results of optimal phosphorylation sites, different effects of Cdc42 interactions, and alternative substrates, those factors fluctuated levels of regulation.

Cervical cancer progression promoted by PAK6 through Wnt/β-catenin signaling pathway activation

As a member of the serine/threonine kinase family, p21-activated kinase 6 (PAK6) has been reported to be involved in numerous cancers. Expression levels of Wnt/β-catenin signaling associate proteins can be modified by PAK6 knockdown, such as downregulation of GSK3β phosphorylation and Cyclin D1 protein, and upregulation of β-catenin phosphorylation and E-cadherin. And overexpression of PAK6 is accompanied by the activation of Wnt/β-catenin signaling pathway. Interaction between PAK6 with GSK3β was indicated by investigation in fluroscence microscopy and Co-IP assays. Those findings suggest that PAK6 may act as a promoter of cervical cancer by activation of the Wnt/β-catenin signaling pathway.

Figure 1. The epigenetic regulation of PAK6 in HCC. (Gong, et al. 2020)

References:

Gong C C, Li T T, Pei D S. PAK6: a potential anti-cancer target. Brazilian Journal of Pharmaceutical Sciences, 2020, 56.
Yang Q, Zhao Y, Chen Y, et al. PAK6 promotes cervical cancer progression through activation of the Wnt/βcatenin signaling pathway. Oncology Letters, 2020, 20(3): 2387-2395.

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