Sharpin promotes hepatocellular carcinoma progression via transactivation of Versican expression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12-12

AUTHORS

Y Tanaka, K Tateishi, T Nakatsuka, Y Kudo, R Takahashi, K Miyabayashi, K Yamamoto, Y Asaoka, H Ijichi, R Tateishi, J Shibahara, M Fukayama, T Ishizawa, K Hasegawa, N Kokudo, K Koike

ABSTRACT

Sharpin (Shank-associated RH domain-interacting protein, also known as SIPL1) is a multifunctional molecule that participates in various biological settings, including nuclear factor-κB signaling activation and tumor suppressor gene inhibition. Sharpin is upregulated in various types of cancers, including hepatocellular carcinoma (HCC), and is implicated in tumor progression. However, the exact roles of Sharpin in tumorigenesis and tumor progression remain largely unknown. Here we report novel mechanisms of HCC progression through Sharpin overexpression. In our study, Sharpin was upregulated in human HCC tissues. Increased Sharpin expression enhanced hepatoma cell invasion, whereas decrease in Sharpin expression by RNA interference inhibited invasion. Microarray analysis identified that Versican, a chondroitin sulfate proteoglycan that plays crucial roles in tumor progression and invasion, was also upregulated in Sharpin-expressing stable cells. Versican expression increased in the majority of HCC tissues and knocking down of Versican greatly attenuated hepatoma cell invasion. Sharpin expression resulted in a significant induction of Versican transcription synergistically with Wnt/β-catenin pathway activation. Furthermore, Sharpin-overexpressing cells had high tumorigenic properties in vivo. These results demonstrate that Sharpin promotes Versican expression synergistically with the Wnt/β-catenin pathway, potentially contributing to HCC development. A Sharpin/Versican axis could be an attractive therapeutic target for this currently untreatable cancer. More... »

PAGES

e277-e277

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/oncsis.2016.76

DOI

http://dx.doi.org/10.1038/oncsis.2016.76

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047167578

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27941932


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29 Wnt/β-catenin pathway
30 Wnt/β-catenin pathway activation
31 activation
32 analysis
33 attractive therapeutic target
34 axis
35 biological settings
36 cancer
37 carcinoma
38 carcinoma progression
39 cell invasion
40 cells
41 chondroitin sulfate proteoglycan
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43 decrease
44 development
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48 hepatocellular carcinoma
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50 hepatoma cell invasion
51 high tumorigenic properties
52 human HCC tissues
53 induction
54 inhibition
55 interference
56 invasion
57 majority
58 mechanism
59 microarray analysis
60 molecules
61 multifunctional molecules
62 novel mechanism
63 overexpression
64 pathway
65 pathway activation
66 progression
67 properties
68 proteoglycans
69 results
70 role
71 setting
72 significant induction
73 stable cells
74 study
75 sulfate proteoglycan
76 target
77 therapeutic target
78 tissue
79 transactivation
80 transcription
81 tumor progression
82 tumorigenesis
83 tumorigenic properties
84 types
85 types of cancer
86 untreatable cancers
87 versican
88 versican expression
89 vivo
90 β-catenin pathway
91 β-catenin pathway activation
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