Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma.
The survival and colonization of tumor cells at new locations involve a variety of complex genetic, epigenetic, and microenvironmental factors. TRIM24 was originally named transcription intermediary factor 1-alpha (TIF1α), which was associated with cellular proliferation and was an oncogene in tumor...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3883694?pdf=render |
| _version_ | 1819133337177948160 |
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| author | Xiao Liu Yu Huang Dinghua Yang Xianghong Li Jiankun Liang Liang Lin Meng Zhang Kebo Zhong Bo Liang Jialu Li |
| author_facet | Xiao Liu Yu Huang Dinghua Yang Xianghong Li Jiankun Liang Liang Lin Meng Zhang Kebo Zhong Bo Liang Jialu Li |
| author_sort | Xiao Liu |
| collection | DOAJ |
| description | The survival and colonization of tumor cells at new locations involve a variety of complex genetic, epigenetic, and microenvironmental factors. TRIM24 was originally named transcription intermediary factor 1-alpha (TIF1α), which was associated with cellular proliferation and was an oncogene in tumor development. Here we provide the first evidence of the expression profile and clinicopathological significance of TRIM24 in patients with hepatocellular carcinoma (HCC). Immunohistochemistry was employed to determine the expression level of TRIM24 in HCC tissues and noncancerous liver tissues. Elevated TRIM24 level was found in 61.4% HCC samples (51/83) correlating with AFP (P = 0.036), poor differentiation (P = 0.004), intrahepatic metastasis (P = 0.004), recurrence (P = 0.000006), and shorter tumor-free survival time (P = 0.002). Small interfering RNA induced down-regulation of TRIM24 promoted apoptosis in HCC cell line HepG2. Moreover, western blotting analysis revealed that knockdown of TRIM24 increased the protein levels of p53, Bax, and Caspase-8, and decreased Bcl-2, Survivin, Cyclin D1, and CDK4. Depletion of TRIM24 decreased Snail, Slug, β-catenin, and Vimentin, and increased E-cadherin expression, which suggested the involvement of TRIM24 in EMT. These results indicated that TRIM24 plays an important role in the pathogenesis of human HCC. |
| first_indexed | 2024-12-22T09:45:41Z |
| format | Article |
| id | doaj.art-591675385ee24afb81c1ca68cf644328 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-22T09:45:41Z |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-591675385ee24afb81c1ca68cf6443282022-12-21T18:30:33ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0191e8546210.1371/journal.pone.0085462Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma.Xiao LiuYu HuangDinghua YangXianghong LiJiankun LiangLiang LinMeng ZhangKebo ZhongBo LiangJialu LiThe survival and colonization of tumor cells at new locations involve a variety of complex genetic, epigenetic, and microenvironmental factors. TRIM24 was originally named transcription intermediary factor 1-alpha (TIF1α), which was associated with cellular proliferation and was an oncogene in tumor development. Here we provide the first evidence of the expression profile and clinicopathological significance of TRIM24 in patients with hepatocellular carcinoma (HCC). Immunohistochemistry was employed to determine the expression level of TRIM24 in HCC tissues and noncancerous liver tissues. Elevated TRIM24 level was found in 61.4% HCC samples (51/83) correlating with AFP (P = 0.036), poor differentiation (P = 0.004), intrahepatic metastasis (P = 0.004), recurrence (P = 0.000006), and shorter tumor-free survival time (P = 0.002). Small interfering RNA induced down-regulation of TRIM24 promoted apoptosis in HCC cell line HepG2. Moreover, western blotting analysis revealed that knockdown of TRIM24 increased the protein levels of p53, Bax, and Caspase-8, and decreased Bcl-2, Survivin, Cyclin D1, and CDK4. Depletion of TRIM24 decreased Snail, Slug, β-catenin, and Vimentin, and increased E-cadherin expression, which suggested the involvement of TRIM24 in EMT. These results indicated that TRIM24 plays an important role in the pathogenesis of human HCC.http://europepmc.org/articles/PMC3883694?pdf=render |
| spellingShingle | Xiao Liu Yu Huang Dinghua Yang Xianghong Li Jiankun Liang Liang Lin Meng Zhang Kebo Zhong Bo Liang Jialu Li Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. PLoS ONE |
| title | Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. |
| title_full | Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. |
| title_fullStr | Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. |
| title_full_unstemmed | Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. |
| title_short | Overexpression of TRIM24 is associated with the onset and progress of human hepatocellular carcinoma. |
| title_sort | overexpression of trim24 is associated with the onset and progress of human hepatocellular carcinoma |
| url | http://europepmc.org/articles/PMC3883694?pdf=render |
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