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Basic Characteristics of Mutations
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Mutation Site
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W182X |
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Mutation Site Sentence
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Among these mutations, sW182* was found to have the most potent oncogenicity. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsense mutation |
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Gene/Protein/Region
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S |
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Standardized Encoding Gene
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S
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Genotype/Subtype
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- |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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Carcinoma, Hepatocellular
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Immune
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- |
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Target Gene
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CA10
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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- |
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Location
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- |
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Literature Information
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PMID
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35800619
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Title
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CA10 is associated with HBV-related hepatocarcinogenesis
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Author
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Chung KM,Chen YT,Hong CC,Chang IC,Lin SY,Liang LY,Chen YR,Yeh CT,Huang SF
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Journal
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Biochemistry and biophysics reports
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Journal Info
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2022 Jul 1;31:101303
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Abstract
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Hepatocellular carcinoma (HCC) is the main threat for the patients infected with hepatitis B virus (HBV), but the oncogenic mechanism of HBV-related HCC is still controversial. Previously, we have found that several HBV surface gene (HBS) non-sense mutations are oncogenic. Among these mutations, sW182* was found to have the most potent oncogenicity. In this study, we found that Carbonic Anhydrase X (CA10) level was specifically increased in sW182* mutant-expressing cells. CA10 overexpression was also associated with HBS nonsense mutation in HBV-related HCC tumor tissues. Transformation and tumorigenesis assays revealed that CA10 had significant oncogenic activity. In addition, CA10 overexpression resulted in dysregulation of apoptosis-related proteins, including Mcl-1, Bcl-2, Bcl-xL and Bad. While searching for the regulatory mechanism of CA10, miR-27b was found to downregulate CA10 expression by regulating its mRNA degradation and its expression was decreased in sW182* mutant cells. Moreover, CA10 overexpression was associated with down-regulation of miR-27b in human HBV-related HCC tumor tissues with sW182* mutation. Therefore, induction of the expression of CA10 through repression of miR-27b by sW182* might be one mechanism involved in HBS mutation-related hepatocarcinogenesis.
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Sequence Data
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-
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