Autor: |
Kuei-Min Chung, Ya-Ting Chen, Chih-Chen Hong, Il-Chi Chang, Si-Ying Lin, Li-Yu Liang, Yi-Rong Chen, Chau-Ting Yeh, Shiu-Feng Huang |
Jazyk: |
angličtina |
Rok vydání: |
2022 |
Předmět: |
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Zdroj: |
Biochemistry and Biophysics Reports, Vol 31, Iss , Pp 101303- (2022) |
Druh dokumentu: |
article |
ISSN: |
2405-5808 |
DOI: |
10.1016/j.bbrep.2022.101303 |
Popis: |
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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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